Free Shipping on All Orders $75 Or More!

Your Trusted Brand for Over 35 Years

Health Protocols

Cancer Treatment: The Critical Factors

How to implement step five

Ask your physician to prescribe one of the following statin drugs to inhibit the activity of Ras oncogenes:
  • Mevacor (lovastatin)
  • Zocor (simvastatin)
  • Pravachol (pravastatin)

Note: Statin drugs may generate adverse side effects. Physician oversight and careful surveillance with monthly blood tests (at least initially) to evaluate liver function, muscle enzymes, and lipid levels are suggested.

In addition to statin drug therapy, consider supplementing with the following nutrients to further suppress the expression of Ras oncogenes:

  • Curcumin: (as highly absorbed BCM-95® extract): 400 – 800 mg daily
  • Fish Oil: 2100 mg of EPA and 1500 mg of DHA daily with meals
  • Green Tea; standardized extract: 725 – 1450 mg of EGCG daily
  • Aged Garlic Extract: 2400 mg daily with meals
  • Vitamin E: 400 – 1000 IU of natural alpha tocopherol along with at least 200 mg of gamma tocopherol daily with meals

Step Six: Correcting Coagulation Abnormalities

Both experimental and clinical data have determined that coagulation disorders are common in patients with cancer. Many cancer patients reportedly have a hypercoagulable state, with recurrent thrombosis (blood clot) due to the impact of cancer cells and chemotherapy on the coagulation cascade (Samuels et al. 1975). Pulmonary embolism (blood clot in the lung) is a particular problem for patients with pancreatic and gastric cancer, colon cancer, and ovarian cancer (Cafagna et al. 1997). Thus, momentum is building for anticoagulant therapy through reports, the vast majority of which are derived from secondary analyses of clinical trials on the treatment of thromboembolism.

Research on low-molecular-weight heparin (LMWH)—an anticoagulant—shows promise in regard to increasing cancer survival rates. Data comparing unfractionated heparin to LMWH indicate that LMWH is equally beneficial if not more beneficial to cancer patients in terms of survival. The improved life expectancy gathered from anticoagulant therapy is not solely a result of the reduced complications from thromboembolism, but also from enzyme interactions, cellular growth modifications, and anti-angiogenic factors (Ahmad 2011; Cosgrove et al. 2002). It appears heparin inhibits the formation of cancer's vascular network by binding to angiogenic promoters (i.e. basic fibroblast growth factor and VEGF) (Mousa 2002).

Another important aspect of anticoagulant therapy involves breaking down fibrin, a coagulation protein found in blood. Cancers employ various strategies to utilize fibrin for their own benefit. For example, fibrin covers cancer cells with a protective coat, hindering recognition by the immune system. In addition, fibrin relays a signal to the cancer to initiate angiogenesis—the growth of new blood vessels. As fibrin encourages a healthy vascular network and tumor growth increases, it sets the stage for metastasis.

German scientists evaluated whether cancer fatalities in women with previously untreated breast cancer were reduced using LMWH therapy. The study showed that breast cancer patients receiving LMWH had a lower rate of mortality during the first 650 days following surgery, compared to women receiving unfractionated heparin. The survival advantage was apparent after even a short course of therapy (von Tempelhoff et al. 2000). In another study of 300 breast cancer patients, none of the trial participants developed metastasis while receiving anticoagulant therapy although 37 (12.3%) died from the disease (Wellness Directory of Minnesota 2002).

Similar advantages were evidenced among small cell lung cancer patients undergoing heparin therapy in conjunction with conventional treatments. When subjects were treated with heparin they enjoyed a better prognosis, with greater numbers of complete responses, longer median survival, and higher survival rates at 1, 2, and 3 years compared to patients who did not receive heparin (Lebeau et al. 1994).

A comprehensive analysis of the data pertaining to all studies published on the impact of heparin treatment on survival in cancer patients determined that treatment with heparin (both unfractionated heparin and LMWH) decreased the risk of death by 23%, compared to those who did not receive heparin (Van Doormaal et al. 2008).

How to Implement Step Six

Ascertain if you are in a hypercoagulable state by having your blood tested for prothrombin time (PT), partial thromboplastin time (PTT), and D-dimers. A hypercoagulable state is suggested if the shortening of the PT and PTT are seen in conjunction with elevation of D-dimers (see table after next paragraph on laboratory tests for hypercoagulability).

If there is any evidence of a hypercoagulable (prethrombotic) state, ask your physician to prescribe the appropriate individualized dose of low-molecular-weight heparin (LMWH). Repeat the prothrombin blood test every 2 weeks.

Lab Tests for Hypercoagulability

Tests routinely available

Results if hypercoagulable

Tests requiring dedicated coagulation laboratory

Results if hypercoagulable

Protime (PT)

Less than normal

Alpha-1 antitrypsin (A1AT)


Partial thromboplastin time (PTT)

Less than normal

Euglobulin clot lysis time (ECLT)


Platelet count (part of CBC)


Factor VIII levels


Step Seven: Maintaining Bone Integrity

Some types of cancer (i.e. breast, prostate, and multiple myeloma) have a proclivity to metastasize to the bone (Hohl 1995; Wang 2000). The result may be bone pain, which also may be associated with weakening of the bone and an increased risk of fractures (Spivak 1994; Caro 2001).

Patients with prostate cancer have been found to have a very high incidence of osteoporosis or osteopenia even before the use of therapies that lower testosterone levels (Cazzola 2000). In settings such as prostate cancer, when excessive bone loss is occurring, there is a release of bone-derived growth factors, such as TGF-beta-1, which has been associated with aggressive prostate cancer (Reis 2011). In turn, prostate cancer cells produce substances such as interleukin-6 (IL-6), which causes effects the further breakdown of bone (Cafagna et al. 1997; Mousa 2002). Thus, a vicious cycle results: bone breakdown, the stimulation of prostate cancer cell growth, and the production of interleukin IL -6 and other cell products, which leads to further bone breakdown.

The administration of any of the drugs called bisphosphonates, such as Aredia, Zometa®, and Fosamax or Actonel can be used to stop this vicious cycle. These agents inhibit excessive bone breakdown and favor bone formation (Zacharski 1984; Zacharski 1987; Chahinian 1989; von Templehoff 2000; Saad F 2009).

The problem that prostate and breast cancer patients face is that bisphosphonate therapy is usually only prescribed for preexisting bone metastasis. If bisphosphonates were administered to those with cancer preventatively, then the risk of bone metastasis could theoretically be reduced (Mystakidou K 2005), though not all studies substantiate this. A study published in 2008 revealed that premenopausal women with early-stage breast cancer (i.e. no bone metastasis) given Zometa® experienced a trend towards decreased bone metastasis and greater survival (Gnant BT 2008). A subsequent study found an improvement in survival in women with breast cancer who were five years past menopause who took Zometa® preventatively. However, premenopausal and perimenopausal women did not experience a survival benefit (Coleman RE, 2010)

Other studies have documented the ability of Zometa® to prevent the onset of bone metastasis. In one study, patients with advanced solid tumors and no evidence of bone metastases were randomized to receive Zometa® or no further treatment. After 12 months, 60% of those receiving Zometa® were free of bone metastasis, compared to only 10% in the control group. After 18 months, 20% of those in the Zometa® group were free of bone metastasis, compared to only 5% in the control group (Mystakidou K 2005). Zometa® has also been shown to benefit those with multiple myeloma when given preventatively, by improving survival and reducing the risk of bone metastasis (Morgan 2010).

The benefits of Zometa® in women with breast cancer are not limited to the prevention of bone metastasis. Many women with breast cancer are given a drug called an aromatase inhibitor. This class of drugs are estrogen blockers and are frequently used in place of tamoxifen in postmenopausal women with estrogen receptor positive breast cancer. Aromatase inhibitors can cause bone loss and can increase the risk of osteoporosis. In addition to preventing bone metastasis, Zometa® has also been shown to protect against the loss of bone density from the use of aromatase inhibitors (Hwang SH 2011).

Note: Bisphosphonate drugs have potentially serious adverse effects. The use of bisphosphonate drugs has been associated with an increased risk of osteonecrosis of the jaw (death and decay of the jaw bone). The incidence of osteonecrosis of the jaw during therapy with Zometa® was found to be 1.3% (Stopeck 2010). This risk is considerably greater in those who had major dental work (i.e. tooth extraction) performed during bisphosphonate use. Individuals should avoid undergoing tooth extractions during therapy with Zometa®. Individuals who use bisphosphonate medications under a physician’s guidance can help reduce their risk of osteonecrosis of the jaw by receiving a dental examination and undergoing any necessary dental procedures such as tooth extractions before initiating drug therapy (Weitzman R. 2007). Those taking bisphosphonate drugs should also take bone-protecting minerals like calcium, magnesium, and boron, along with vitamins D and K.

Additionally, people treated with Zometa® have an increased risk of atrial fibrillation, or irregular heart rhythm causing the heart to pump blood less efficiently, potentially resulting in pulmonary edema (fluid in the lungs), congestive heart failure, stroke, or death. A study showed that 2.5-3% of patients taking bisphosphonates developed atrial fibrillation and 1-2% developed serious atrial fibrillation, with complications including hospitalization or death (Heckbert, SR et al. 2008).

It should be noted that 6.9% of individuals treated with Zometa® experienced kidney toxicity. Zometa® should be used with caution in those with preexisting kidney disease and is contraindicated in those with severe kidney disease (Stopeck 2010).

New research has produced an alternative to Zometa® for the treatment of bone metastasis. Denosumab (Xgeva®) is a monoclonal antibody that inhibits osteoclastic-mediated bone resorption by binding to osteoblast-produced RANKL. By reducing RANKL binding to the osteoclast receptor RANK, bone resorption and turnover decrease (Miller 2009). Denosumab has recently been shown to be more effective than Zometa® in the treatment of bone metastasis. In one study, 1904 men with prostate cancer with bone metastasis were randomized to receive Zometa® or Denosumab. The time it took for a subsequent bone metastasis related event (i.e. fracture, spinal cord compression, or radiation/surgery to bone) was longer in the denosumab group, demonstrating the superiority of denosumab over Zometa® (Fizazi K 2011).

Denosumab was also compared to Zometa® in women with breast cancer with bone metastasis. This trial found that Denosumab was superior to Zometa® in delaying the time to bone metastasis related events (Stopeck 2010). Unfortunately, osteonecrosis of the jaw is also a side effect of treatment with Denosumab. Indeed, the incidence of osteonecrosis of the jaw was slightly higher with Denosumab compared to Zometa®. As with Zometa®, renal toxicity has been associated with the use of Denosumab.

A COX-2 inhibitor drug presents another option for the prevention of bone metastasis. As discussed in Step Four of this protocol: Inhibiting COX-2 Enzyme, breast cancer patients treated with a COX-2 inhibitor drug had a 90% reduced risk of developing bone metastases compared to those not treated with a COX-2 inhibitor.

Life Extension advises that the status of bone integrity should be evaluated periodically by means of a quantitative computerized tomography bone mineral density study—called QCT. At the very least, this should be done annually. We prefer to use the QCT scan over the standard DEXA scan since the QCT is not falsely affected by arthritis or calcifications in blood vessels that are commonly seen in individuals over age 50. It is fairly common to see patients with a normal DEXA scan and yet the QCT scan will be blatantly abnormal. The radiation exposure with QCT is only marginally greater than with DEXA scan.

QCT testing sites possibly near you can be found via Mindways, Inc. at (877) 646-3929 or Image Analysis at (800) 548-4849.

Tests that assess bone breakdown are inexpensive and involve a simple urine collection. One such accurate test of bone resorption is called DPD (deoxypyridinoline). This test provides information on excessive bone breakdown. The deoxypyridinoline (DPD) cross links urine test can be ordered through the Life Extension by calling 1-800-226-2370.

How to implement step Seven

If you have a type of cancer with a proclivity to metastasize to the bone (i.e. multiple myeloma, breast, or prostate), consider speaking to your oncologist regarding Zometa® or Denosumab. If either of these medications are contraindicated, then consider the COX-2 inhibitor drug Celebrex®. Please see step four of this protocol for a complete discussion of COX-2 inhibition.

One must always weigh the risks versus the benefits when evaluating a given treatment. This is certainly the case when considering the use of Zometa®, Denosumab, or Celebrex® for the prevention of bone metastasis. Given the excellent prognosis and low risk of bone metastasis, Life Extension does not recommend the use of Zometa®, Denosumab, or Celebrex® for women with stage 1 and stage 2A breast cancer. With higher risk cancer, the benefits of these medications likely outweigh the risks. Life Extension recommends the use of medications for the prevention of bone metastasis in women with stage 2B, stage 3, or stage 4 breast cancers.

With regard to prostate cancer, a large percentage of men will be cured with surgery or radiation. Treatment failure is easily detected by a rising PSA after initial treatment. Furthermore, it usually takes several years for bone metastasis to form once a rising PSA has detected treatment failure. This prolonged time frame for the formation of bone metastasis allows for the use of proactive therapies once treatment failure has been detected by a rising PSA. For this reason, Life Extension recommends the use of medications for the prevention of bone metastasis only when treatment failure has been detected by a rising PSA after initial treatment. An exception to this recommendation would be men with osteoporosis receiving androgen deprivation therapy for their initial treatment. Androgen deprivation therapy can result in further loss of bone density. Given that Zometa® can protect against the loss of bone density, the benefits of using this medication may outweigh the risks in men with osteoporosis receiving long-term androgen deprivation therapy.

Since excessive bone breakdown releases growth factors into the bloodstream that can fuel cancer cell growth, the DPD urine test should be done every 60-90 days to detect bone loss. A QCT bone density scan should be done annually. If either of these tests indicates bone loss, ask your physician to initiate bisphosphonate therapy.

To support bone integrity, the use of bone-supporting nutrients is highly recommended. These include optimal amounts of vitamin K, vitamin D, calcium, magnesium, boron, and silica. Please see the Osteoporosis protocol for a detailed discussion of the use and dose of these nutritients for bone support.

Step Eight: Inhibiting Angiogenesis

Angiogenesis—the growth of new blood vessels—is critical during fetal development but occurs minimally in healthy adults. Exceptions occur during wound healing, inflammation, following a myocardial infarction, in female reproductive organs, and in pathologic conditions such as cancer (Shammas 1993; Suh 2000).

Angiogenesis is a strictly controlled process in the healthy adult human body, a process regulated by endogenous angiogenic promoters and inhibitors. Dr. Judah Folkman, the father of the angiogenesis theory of cancer stated, "Blood vessel growth is controlled by a balancing of opposing factors. A tilt in favor of stimulators over inhibitors might be what trips the lever and begins the process of tumor angiogenesis" (Cooke 2001).

Solid tumors cannot grow beyond the size of a pinhead without inducing the formation of new blood vessels to supply the nutritional needs of the tumor (Folkman J 1971). Since rapid vascularization and tumor growth appear to occur concurrently, interrupting the formation of new blood vessels is paramount to overcoming the malignancy (Cao Y 2008).

Tumor angiogenesis results from a cascade of molecular and cellular events, usually initiated by the release of angiogenic growth factors. At a critical phase in the growth of a cancer, signal molecules are secreted from the cancer to nearby endothelial cells to activate new blood vessel growth. These angiogenic growth factors diffuse in the direction of preexisting blood vessels, encouraging the formation of new blood vessel growth (Folkman 1992 b; Folkman et al. 1992a). VEGF and basic fibroblast growth factors are expressed by many tumors and appear to be particularly important for angiogenesis (NIH/NCI 1998).

A number of natural substances, such as curcumin, green tea, N-acetyl-cysteine (NAC), resveratrol, grape seed-skin extract, and vitamin D have anti-angiogenic properties. For further discussion, see the protocol: Cancer Adjuvant Therapy.

FDA has approved an anti-angiogenesis drug called Avastin® (bevacizumab), but it has demonstrated severe side effects and often only mediocre efficacy. Several other drugs inhibit angiogensis as secondary mechanisms and are sometimes utilized in cancer therapy. These included sorafenib, sunitinb, pazopanib, and everolimus. These options should be discussed with a healthcare professional because these drugs may cause considerable side effects, and are only FDA approved for specific types of cancer.

How to implement Step Eight

  • There are clinical trials using other anti-angiogenesis agents. Log on to to find out if you are eligible to participate.
  • Several nutrients have demonstrated potential antiangiogenesis effects such as green tea extract and curcumin.
    • Green tea: standardized extract: 725 – 1450 mg daily
    • Curcumin: (as highly absorbed BCM-95®): 400 – 800 mg daily
    • Vitamin D: 5000 – 8000 IU daily (depending on blood levels)
    • Grape extract (seed and skin): 150 – 300 mg daily
    • N-Acetyl cysteine: 600 – 1200 mg daily

Step Nine: Inhibiting the 5-lipoxygenase (5-LOX) Enzyme

As discussed in Step 4 of this protocol: Inhibiting the Cyclooxygenase-2 (COX-2) Enzyme, the scientific literature has demonstrated that inflammation plays a pivotal role in the formation and progression of cancer.

The 5-lipoxygenase (5-LOX) enzyme is another inflammatory enzyme that can contribute to the formation and progression of cancer. Arachidonic acid--a saturated fat found in high concentrations in meat and dairy products—promotes elevation of the 5-LOX enzyme. A growing number of studies have documented that 5-LOX directly stimulates prostate cancer cell proliferation via several well-defined mechanisms (Ghosh et al. 2004; Moretti et al. 2004; Hassan et al. 2006; Matsuyama et al. 2004; Kelavkar et al. 2004; Gupta et al. 2001; Kelavkar et al. 2001; Ghosh et al. 1997; Gao et al. 1995). In addition, arachidonic acid is metabolized by 5-LOX to 5-HETE, a potent survival factor that prostate cancer cells utilize to escape destruction. (Matsuyama et al. 2004; Sundaram et al. 2006; Myers et al. 1999; Nakao-Hayashi et al. 1992; Cohen et al. 1991).

In response to arachidonic acid overload, the body increases its production of enzymes like 5-lipooxygenase (5-LOX) to degrade arachidonic acid. Not only does 5-LOX directly stimulate cancer cell propagation (Ghosh 2003; Jiang et al. 2006; Yoshimura et al. 2004; Zhang et al. 2006; Soumaoro et al. 2006; Hayashi et al. 2006; Matsuyama et al. 2004; Hoque et al. 2005; Hennig et al. 2002; Ding et al. 1999; Matsuyama et al. 2005), but the breakdown products that 5-LOX produces from arachidonic acid (such as leukotriene B4, 5-HETE, and hydroxylated fatty acids) cause tissue destruction, chronic inflammation, and increased resistance of tumor cells to apoptosis (programmed cell destruction) (Hassan 2006; Sundaram 2006; Zhi 2003; Penglis 2000; Rubinsztajn 2003; Subbarao 2004; Hu 2013).

Based on studies showing that consumption of foods rich in arachidonic acid is greatest in regions with high incidences of prostate cancer (Moretti 2004; Hassan 2006; Ghosh 1997; Ghosh 2003), scientists sought to determine how much of the 5-LOX enzyme is present in malignant versus benign prostate tissues. Using prostate biopsy samples, the researchers found that 5-LOX levels were an astounding six-fold greater in malignant prostate tissues compared to benign tissues. This study also found that levels of 5-HETE were 2.2-fold greater in malignant versus benign prostate tissues (Gupta 2001). The scientists concluded this study by stating that selective inhibitors of 5-LOX may be useful in the prevention or treatment of patients with prostate cancer.

As the evidence mounts that consuming saturated fats increase prostate cancer risk, scientists are evaluating the effects of 5-LOX on various growth factors involved in the progression, angiogenesis, and metastasis of cancer cells. One study found that 5-LOX activity is required to stimulate prostate cancer cell growth by epidermal growth factor (EGF) and other cancer cell proliferating factors produced in the body. When 5-LOX levels were reduced, the cancer cell stimulatory effect of EGF and other growth factors was diminished (Hassan 2006).

In a mouse study, an increase in 5-LOX resulted in a corresponding increase in vascular endothelial growth factor (VEGF), a key growth factor that tumor cells use to stimulate new blood vessel formation (angiogenesis) into the tumor. 5-LOX inhibitors were shown to reduce tumor angiogenesis along with a host of other growth factors (Ye 2004). Chronic inflammation is tightly linked to the induction of aberrant angiogenesis used by cancer cells to facilitate the growth of new blood vessels (angiogenesis) into tumors (Rajashekhar 2006).

In both androgen-dependent and androgen-independent human prostate cancer cell lines, the inhibition of 5-lipoxygenase (5-LOX) has consistently been shown to induce rapid and massive apoptosis (cancer cell destruction) (Moretti 2004; Ghosh 2003; Hazai 2006; Ghosh 1998; Yang 2003; Anderson 1998).

As humans age, chronic inflammatory processes can cause the over-expression of 5-LOX in the body. Excess 5-LOX may contribute to the development and progression of prostate cancer in aging males (Steinhilber 2010).

Based on the cumulative knowledge that 5-LOX can promote the invasion and metastasis of prostate cancer cells, it would appear advantageous to take aggressive steps to suppress this lethal enzyme. A critical approach to decreasing 5-LOX activity in the body is to decrease the consumption of saturated and omega-6 fats that contain high concentrations of arachidonic acid and high glycemic carbohydrates that contribute to arachidonic acid formation. Another worthwhile approach is to supplement with fish oil, which reduces 5-LOX activity in the body (Taccone-Gallucci 2006; Calder 2003). Studies show that lycopene and saw palmetto extract also help to suppress 5-LOX (Hazai 2006; Jian 2005; Campbell 2004; Wertz 2004; Binns 2004; Kim 2002; Giovannucci 2002; Vogt 2002; Bosetti 2000; Blumenfeld 2000; Agarwal 2000; Gann 1999; Giovannucci 1995; Hill 2004; Paubert-Braquet 1997). The suppression of 5-LOX by these nutrients may partially account for their favorable effects on the prostate gland.

Specific extracts from the boswellia plant selectively inhibit 5-lipoxygenase (5-LOX) (Safayhi 1997; Safayhi 1995). In several well-controlled human studies, boswellia has been shown to be effective in alleviating various chronic inflammatory disorders (Kimmatkar 2003; Ammon 2002; Wallace 2002; Gupta 2001; Gerhardt 2001; Gupta 1998; Kulkarni 1991; Park 2002; Liu 2002; Syrovets 2000). Scientists have discovered that the specific constituent in boswellia responsible for suppressing 5-LOX is AKBA (3-O-acetyl-11-keto-B-boswellic acid). Boswellia-derived AKBA binds directly to 5-LOX and inhibits its activity.70 Other boswellic acids only partially and incompletely inhibit 5-LOX (Safayhi 1995; Sailer 1996).

Researchers have discovered how to obtain an economically viable boswellia extract standardized to contain a greater than 20% concentration of AKBA. A novel boswellia extract has been developed that is 52% more bioavailable compared to standard boswellia extracts (Sengupta 2011; Krishnaraju 2010) thus providing a greater opportunity to suppress deadly 5-LOX and other cancer-promoting byproducts of arachidonic acid. This more bioavailable AKBA extraction discovery was patented and given the trademark name AprèsFlex™.

How to implement Step Nine

Decrease the consumption of saturated and omega-6 fats that contain high concentrations of arachidonic acid, such as meats, dairy products, and egg yolks, along with high-glycemic carbohydrates.

Consider supplementing with the following nutrients to suppress 5-LOX enzyme activity:

  • AprèsFlex™: 100 to 400 mg daily
  • Fish Oil: 2100 mg of EPA and 1500 mg of DHA daily with meals
  • Lycopene: 30 mg daily with meals
  • Curcumin (as highly absorbed BCM-95®): 400 – 800 mg daily

Step Ten: Inhibiting Cancer Metastasis

The surgical removal of the primary tumor has been the cornerstone of treatment for the great majority of cancers. The rationale for this approach is straightforward: if you can get rid of the cancer by simply removing it from the body, then a cure can likely be achieved. Unfortunately, this approach does not take into account that after surgery the cancer will frequently metastasize (spread to different organs). Quite often, the metastatic recurrence is far more serious than the original tumor. In fact, for many cancers, it is the metastatic recurrence—and not the primary tumor—that ultimately proves to be fatal (Bird 2006).

One mechanism by which surgery increases the risk of metastasis is by enhancing cancer cell adhesion (Dowdall 2002). Cancer cells that have broken away from the primary tumor utilize adhesion to boost their ability to form metastases in distant organs. These cancer cells must be able to clump together and form colonies that can expand and grow. It is unlikely that a single cancer cell will form a metastatic tumor, just as one person is unlikely to form a thriving community. Cancer cells use adhesion molecules—such as galectin-3—to facilitate their ability to clump together. Present on the surface of cancer cells, these molecules act like velcro by allowing free-standing cancer cells to adhere to each other (Raz 1987).

Cancer cells circulating in the bloodstream also make use of galectin-3 surface adhesion molecules to latch onto the lining of blood vessels (Yu 2007). The adherence of circulating tumor cells (CTC) to the blood vessel walls is an essential step for the process of metastasis. A cancer cell that cannot adhere to the blood vessel wall will just continue to wander through the blood stream incapable of forming metastases. Unable to latch onto the wall of the blood vessel, these circulating tumor cells become like "ships without a port" and are unable to dock. Eventually, white blood cells circulating in the bloodstream will target and destroy the CTC. If the CTC’s successfully bind to the blood vessel wall and burrow their way through the basement membrane, they will then utilize galectin-3 adhesion molecules to adhere to the organ to form a new metastatic cancer (Raz 1987).

Regrettably, research has shown that cancer surgery increases tumor cell adhesion (ten Kate 2004). Therefore, it is critically important for the person undergoing cancer surgery to take measures that can help to neutralize the surgery-induced increase in cancer cell adhesion.

Fortunately, a natural compound called modified citrus pectin (MCP) can do just that. Citrus pectin—a type of dietary fiber—is not absorbed from the intestine. However, modified citrus pectin has been altered so that it can be absorbed into the blood and exert its anti-cancer effects. The mechanism by which modified citrus pectin inhibits cancer cell adhesion is by binding to galectin-3 adhesion molecules on the surface of cancer cells, thereby preventing cancer cells from sticking together and forming a cluster (Nangia-Makker 2002). Modified citrus pectin can also inhibit circulating tumor cells from latching onto the lining of blood vessels. This was demonstrated by an experiment in which modified citrus pectin blocked the adhesion of galectin-3 to the lining of blood vessels by an astounding 95%. Modified citrus pectin also substantially decreased the adhesion of breast cancer cells to the blood vessel walls (Nangia-Makker 2002).

After these exciting findings in animal research, modified citrus pectin was then put to the test in men with prostate cancer. In this trial, 10 men with recurrent prostate cancer received modified citrus pectin (14.4 g per day). After one year, a considerable improvement in cancer progression was noted, as determined by a reduction of the rate at which the prostate-specific antigen (PSA) level increased (Guess 2003). This was followed by a study in which 49 men with prostate cancer of various types were given modified citrus pectin for a four-week cycle. After two cycles of treatment with modified citrus pectin, 22% of the men experienced a stabilization of their disease or improved quality of life; 12% had stable disease for more than 24 weeks. The authors of the study concluded that "MCP (modified citrus pectin) seems to have positive impacts especially regarding clinical benefit and life quality for patients with far advanced solid tumor" (Jackson 2007).

In addition to modified citrus pectin, a well-known over-the-counter medication can also play a pivotal role in reducing cancer cell adhesion. Cimetidine—commonly known as Tagamet®—is a drug historically used to alleviate heartburn. A growing body of scientific evidence has revealed that cimetidine also possesses potent anti-cancer activity.

Cimetidine inhibits cancer cell adhesion by blocking the expression of an adhesive molecule—called E-selectin—on the surface of cells lining blood vessels (Eichbaum 2011). Cancers cells latch onto E-selectin in order to adhere to the lining of blood vessels (Eichbaum 2011). By preventing the expression of E-selectin, cimetidine significantly limits the ability of cancer cell adherence to the blood vessel walls. This effect is analogous to removing the velcro from the blood vessels walls that would normally enable circulating tumor cells to bind.

Cimetidine’s potent anti-cancer effects were clearly displayed in a report published in the British Journal of Cancer in 2002. In this study, 64 colon cancer patients received chemotherapy with or without cimetidine (800 mg per day) for one year. The 10-year survival for the cimetidine group was almost 90%. This is in stark contrast to the control group, which had a 10-year survival of only 49.8%. Remarkably, for those patients with a more aggressive form of colon cancer, the 10-year survival was 85% in those treated with cimetidine compared to a dismal 23% in the control group (Matsumoto 2002). The authors of the study concluded, "Taken together, these results suggested a mechanism underlying the beneficial effect of cimetidine on colorectal cancer patients, presumably by blocking the expression of E-selectin on vascular endothelial [lining of blood vessels] cells and inhibiting the adhesion of cancer cells." These findings are supported by another study with colorectal cancer patients wherein cimetidine given for just seven days at the time of surgery increased three-year survival from 59% to 93% (Adams 1994).

Another major contributor to cancer metastasis is immune dysfunction; primarily that which occurs immediately following a surgical procedure such as removal of a primary tumor (Shakhar 2003). Specifically, surgery suppresses the number of specialized immune cells called natural killer (NK) cells, which are a type of white blood cell tasked with seeking out and destroying cancer cells.

To illustrate the importance of NK cell activity in fighting cancer, a study published in the journal Breast Cancer Research and Treatment examined NK cell activity in women shortly after surgery for breast cancer. The researchers reported that low levels of NK cell activity were associated with an increased risk of death from breast cancer (Eichbaum 2011). In fact, reduced NK cell activity was a better predictor of survival than the actual stage of the cancer. In another alarming study, individuals with reduced NK cell activity before surgery for colon cancer had a 350% increased risk of metastasis during the following 31 months (Koda 1997).

One prominent natural compound that can increase NK cell activity is PSK, (protein-bound polysaccharide K) a specially prepared extract from the mushroom Coriolus versicolor. PSK has been shown to enhance NK cell activity in multiple studies (Fisher 2002; Garcia-Lora 2001). PSK’s ability to enhance NK cell activity helps to explain why it has been shown to dramatically improve survival in cancer patients. For example, 225 patients with lung cancer received radiation therapy with or without PSK (3 grams per day). For those with more advanced Stage 3 cancers, more than three times as many individuals taking PSK were alive after five years (26%), compared to those not taking PSK (8%). PSK more than doubled five-year survival in those individuals with less advanced Stage 1 or 2 disease (39% vs.17%) (Hayakawa 1997).

In a 2008 study, a group of colon cancer patients were randomized to receive chemotherapy alone or chemotherapy plus PSK, which was taken for two years. The group receiving PSK had an exceptional 10-year survival of 82%. Sadly, the group receiving chemotherapy alone had a 10-year survival of only 51% (Sakai 2008). In a similar trial reported in the British Journal of Cancer, colon cancer patients received chemotherapy alone or combined with PSK (3 grams per day) for two years. In the group with a more dangerous Stage 3 colon cancer, the five-year survival was 75% in the PSK group. This compared to a five-year survival of only 46% in the group receiving chemotherapy alone (Ohwada 2004). Additional research has shown that PSK improves survival in cancers of the breast, stomach, esophagus, and uterus as well (Okazaki 1986; Nakazato 1994; Toi 1992).

How to Implement Step Ten

The following three novel compounds have shown efficacy in inhibiting several mechanisms that contribute to cancer metastasis. It is especially important to consider these compounds during the perioperative period (period before and after surgery), because a known consequence of surgery is an enhanced proclivity for metastasis.

  • Modified Citrus Pectin: 15 grams daily, in three divided doses
  • Cimetidine: 800 mg daily, in two divided doses
  • Coriolus versicolor; standardized extract: 1200 – 3600 mg daily

Disclaimer and Safety Information

This information (and any accompanying material) is not intended to replace the attention or advice of a physician or other qualified health care professional. Anyone who wishes to embark on any dietary, drug, exercise, or other lifestyle change intended to prevent or treat a specific disease or condition should first consult with and seek clearance from a physician or other qualified health care professional. Pregnant women in particular should seek the advice of a physician before using any protocol listed on this website. The protocols described on this website are for adults only, unless otherwise specified. Product labels may contain important safety information and the most recent product information provided by the product manufacturers should be carefully reviewed prior to use to verify the dose, administration, and contraindications. National, state, and local laws may vary regarding the use and application of many of the treatments discussed. The reader assumes the risk of any injuries. The authors and publishers, their affiliates and assigns are not liable for any injury and/or damage to persons arising from this protocol and expressly disclaim responsibility for any adverse effects resulting from the use of the information contained herein.

The protocols raise many issues that are subject to change as new data emerge. None of our suggested protocol regimens can guarantee health benefits. The publisher has not performed independent verification of the data contained herein, and expressly disclaim responsibility for any error in literature.