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Cancer Adjuvant Therapy Protocol

 

Nobel laureate Otto Warburg, Ph.D., discovered in 1955 that cancer cells use glucose for fuel. But glucose accomplishes another strategic maneuver that strongly favors the cancer: it immobilizes internal defenses, the actions of the immune system. A study involving 10 healthy human volunteers assessed fasting blood glucose levels and the phagocytic index of neutrophils, a type of white blood cell. Glucose, fructose, sucrose, honey, and orange juice all significantly decreased the capacity of neutrophils to engulf bac-teria. A diet structured away from sugars deprives cancer of its energy and increases the reliability of the immune response.

Dr. Jeff Bland advises selecting foodstuffs low on the glycemic index to avoid gratifying the tumor's appetite. The glycemic index lists the relative speed at which different foods are digested and raise blood sugar levels. Each food is compared to the effect of the same amount of pure glucose on the body's blood sugar curve. Glucose itself has a glycemic index rating of 100. Foods that are broken down and raise blood glucose levels quickly have higher ratings. The closer to 100, the more the food resembles glucose. The lower the rating, the more gradually that food affects blood sugar levels.

Common foods have the following glycemic ratings: baked potatoes, 95; white bread, 95; mashed potatoes, 90; chocolate candy bar, 70; corn, 70; boiled potatoes, 70; bananas, 60; white pasta, 55; peas, 50; unsweetened fruit juice, 40; rye bread, 40; lentils, 30; soy, 15; green vegetables; and tomatoes, < 15.

Note: The glycemic index should not be relied upon without factoring in the glycemic load, which is the glycemic index of a food times its carbohydrate content in grams, a concept developed at Harvard School of Public Health in 1997. Carrots, for instance, have a high glycemic index, but a very low glycemic load. This means that carrots consumed in moderation usually do not present a problem. Refer to the Obesity protocol for complete information about the glycemic index load.

An admonition, based more on folk medicine than scientific certainty, to avoid the white foods (all sugar-containing foods, as well as rice, and white flour and flour-based products) appears to have validity when applied to the glycemic index. A diet structured principally around carbohydrates that promotes hyperglycemia (high blood sugar level) and hyperinsulinemia (high blood insulin level) provides an environment that feeds the fire of cancer. High blood insulin levels drive protein L-Tyrosine kinase (leading to cell division) and high blood glucose metabolically feeds cancer cells, a difficult scenario to overcome. On the other hand, a diet centered on fiber-, vitamin-, and mineral-rich foods that causes no blood glucose rise or insulin rush is an excellent target for healthy eating.

The American Journal of Medical Science recently reported that diseases such as obesity and diabetes mellitus (often characterized by hyperinsulinemia) are associated with an increased risk of endometrial, colorectal, and breast cancers. The mechanisms underlying insulin-mediated neoplasias appear to include enhanced DNA synthesis (with the resultant tumor cell growth), inhibited apoptosis, and an altered sex hormone milieu. The reduced insulin levels seen with physical activity, weight loss, and a high fiber diet may in fact account for the decreased cancer incidence observed in individuals who maintain normal glucose and insulin levels (Gupta et al. 2002). Comment: Reducing blood insulin levels has resulted in remarkable improvements in men with prostate disease, with a concurrent drop in PSA levels.

Unfortunately, glucose modulation is an underutilized component of cancer treatment. Some aspects of traditional treatments actually contribute to higher blood levels of glucose. For example, consider hospital meals, often favoring sugar-based foodstuffs. In addition, if the patient is on an IV solution, the infusion is largely dextrose based, feeding the cancer and perpetuating its growth. An irate oncologist recently commented: "Surely, the very least a cancer patient can expect is the omission of long-term glucose infusions, an act almost certain to nurture the tumor and worsen outcome."

The American Cancer Society believes that 30% of all cancer is due to inadequate consumption of vegetables and fruits. About 91% of Americans fail to achieve target recommendations, that is, 5 vegetable servings a day or 2-3 pounds a week. Asians who consume from 15-20 servings of fruits and vegetables a day have a much lower incidence of some cancers.

Vegetables of the cruciferous family are the focus of a worldwide effort to fully isolate the anticarcinogenic constituents of Brassica plants. Italian researchers contributed, showing that glucosinolates (appearing in cruciferous vegetables) can inhibit, retard, or even reverse experimental multistage carcinogenesis (Fimognari et al. 2002). As enzymatic processes hydrolyze glucosinolates, isothiocyanates are released, including sulphoraphane. Sulphoraphane wields a strong arm against cancer, promoting apoptosis, inducing Phase II detoxification enzymes, increasing p53 and participating in the regulatory mechanisms of the cell's growth cycle. Necrosis (localized death of diseased tissues) is typically observed after prolonged exposure to elevated doses of sulphoraphane.

For the last several years, researchers at Johns Hopkins University have urged the inclusion of broccoli sprouts in the diet. According to Dr. Paul Talalay, broccoli sprouts have 20-50 times more anticancer sulphoraphanes than grown vegetables (Fahey et al. 1997). Eating a few tablespoons of sprouts daily can supply the same amount of chemoprotection as 1-2 pounds of broccoli eaten weekly (Talalay 1997). Findings reported at the Proceedings of the National Academy of Sciences (May 28, 2002) also showed that broccoli sprouts contain a chemical that kills H. pylori, even in antibiotic-resistant conditions. The release of anticarcinogenic chemicals from Brassica vegetables is a sequential process that occurs as the plant tissue is broken down. Indole-3-carbinol (I3C), a product of cruciferous metabolism, is referred to as a secondary metabolite, meaning it is not found in a preformed state in the vegetables. Rather, I3C is formed after myrosinase (an enzyme inherent to the plant) is exposed to a phytochemical in the vegetable (glucobrassicin), a glucosinolate that subsequently delivers indole-3-carbinol. This occurs only when vegetable cells are crushed or eaten, a process known as enzymatic hydrolysis. I3C, thus formed, is then broken down in the presence of stomach acid to various byproducts including diindolylmethane (DIM), another powerful defense against cancer (Lukaczer 2001). Generally speaking, it appears highly possible that the breakdown products of I3C may be delivering as much protection as I3C itself (Katchamart et al. 2001; Lukaczer 2001; Lord et al. 2002).

An undesirable effect is the conversion of estrone to a carcinogenic material called 16-alpha hydroxy-estrone that damages DNA and inhibits apoptosis. The ratio of 2-hydroxyestrone to 16-hydroxyestrone indicates a woman's risk for developing breast and ovarian cancer. Levels of 2-hydroxyestrone are typically higher in women who do not get cancer; 16-hydroxyestrone is higher in women who do. When breast cancer cells are treated with I3C (in vitro) 90% of cells undergo growth inhibition, whether estrogen positive or negative (Galland 2000).

Researchers in Denmark showed that broccoli (500 grams for 12 days) increased the average 2 alpha-hydroxyestrone:16 alpha-hydroxyestrone ratio 29.5% (Kall et al. 1997). Hence, consuming vegetables rich in indole-3-carbinol gives hope that as 2-hydroxyestrone increases, cancers will be decreased in both men and women. The ability of I3C to neutralize estrogen metabolites as well as to block aflatoxin (a mycotoxin that promotes prostate cancer) makes cruciferous vegetables equally important to men.

By inhibiting protein kinases and other growth factors, restoring p21 activity, and encouraging apoptosis, I3C appears an effective chemopreventive/therapeutic agent against many types of malignancies (Chinni et al. 2001; Roman-Gomez et al. 2002). Evidencing its benefits, I3C slashed the incidence of cervical cancer from 76-8% in laboratory mice (Jin et al. 1999), and administered in union with tamoxifen, I3C inhibited the growth of estrogen-dependent human MCF-7 breast cancer more effectively than either agent used alone (Cover et al. 1999).

Illustrative of the worth attributed cruciferous vegetables, at a scientific conference, physicians were chastised (referred to as derelict) if they were not stressing the value of Brassica vegetables in their patients' diets. If vegetables providing I3C are in short supply in your diet, indole-3-carbinol capsules are available. For those under 120 pounds, one 200-mg capsule taken 2 times a day is suggested; those between 120-180 pounds should take 200 mg 3 times a day, while those over 180 pounds should take 200 mg twice a day. If the diet generally lacks adequate amounts of vegetables, powdered vegetable extracts are available. An example is PhytoFood. A suggested dosage for cancer patients is 1-2 tbsp daily (with food).

Cholesterol (Can It Be Too Low?)
Hypocholesterolemia (abnormally low levels of cholesterol) has been shown in several epidemiological studies to be related to increased mortality from human cancer. A study reported in the International Journal of Molecular Medicine evaluated cholesterol and triglyceride levels in 135 patients with squamous cell and small cell lung carcinoma. All lung cancer patients had higher rates of hypocholesterolemia as well as lower triglyceride levels compared to a healthy control group. Total cholesterol concentrations were lower in both histological types, but triglyceride levels were lower only in patients with squamous cell lung cancer (Siemianowicz et al. 2000).

An article in Hematology and Oncology reported that 90% of 83 patients with acute myeloid leukemia were hypocholesterolemic (Zyada et al. 1990). Additionally, another article in the European Journal of Haemtology reported that remission in acute myelogenous leukemia was associated with a significant increase in cholesterol levels in those patients with low cholesterol concentrations or high leukocyte counts at diagnosis (Reverter et al. 1988).

Various reports have recently emerged showing that low cholesterol levels are associated with higher death rates (particularly among elderly people), due to mortality from cancer and infection (Weverling-Rijnsburger et al. 1997; Schatz et al. 2001). These findings raise concerns regarding hypocholesterolemic drug therapy and diet manipulation to drastically lower cholesterol levels in a subset of the population.


STRESS AND CANCER

Few events are as stressful as a diagnosis of cancer. As the stress level increases, the outpouring of the adrenal cortex hormone (cortisol) also increases. Stanford University doctors found that women with breast cancer who had abnormal cortisol rhythms survived an average of 3.2 years, while those with normal rhythms survived an average of 4.5 years (more than a year longer). The difference in survival times began to emerge about 1 year after the testing and continued for at least 6 additional years (Richter 2000). As surely as an outpouring of cortisol hastens a cancer patient's demise, chronically elevated cortisol may have preceded the diagnosis of cancer.

Animal studies, mostly involving rats, have built the case for stress as a causal factor in cancer. The onset of cancer appears similarly allied in humans, with the immune system highly responsive to emotional pitfalls. It is well established that when the individual is emotionally challenged, cancer has a significant advantage. The same scenario holds true for bacterial and viral infections.

Psychobiologist Shamgar Ben-Eliyahu, Ph.D., has been working for the past decade on stress, tumor development, and the activity of NK cells (Ben-Eliyahu et al. 2000). Considering all immune system cells, NK cells show the strongest activity in preventing metastasis and the strongest response to stress. Ben-Eliyahu showed that even short-term stress decreases NK cell activity in laboratory animals, significantly increasing the risk of certain types of cancer and metastasis. Gender plays a significant role in the NK cell response to stress, with men more adversely affected than women (Irwin 2000). A recent study also showed that the stress of abdominal surgery promotes the growth of cancerous tumors in rats, a sequence thought orchestrated by NK cell suppression (Ben-Eliyahu et al. 1999).

According to Candace Pert, Ph.D. (in Molecules of Emotion), "The immune system has receptors for every peptide we identified." High levels of neuropeptide-gamma are observed in the bloodstream of depressed individuals, an elevation synonymous with immune suppression (Ader et al. 1981; Scanlan et al. 2001). Macrophage (pathogen scavengers) has receptor sites that attract endorphins (mood enhancers with analgesic traits). Researchers have shown that with the right emotional programming, white blood cells swim through the bloodstream with determination; conversely, under stress, immune competence falters, and the immune attack becomes lethargic.

In 1998, researchers from Ohio State University found that breast cancer patients with the most anxiety had a weaker immune response and were less equipped to fight the disease. The following stress-associated situations and personality types are associated with breast cancer: (1) the use of denial or repression as a coping strategy, (2) an experience of separation or loss, (3) a history of stressful life experiences, (4) a tendency toward melancholy and hopelessness (this trait has, since antiquity, been associated with uterine and breast cancers), and (5) a personality type characterized by conflict avoidance. It is theorized that the genes that cause one to avoid conflict are the same genes that increase susceptibility to cancer (Goodkin et al. 1986; Darmon 1993; ABC News 2000).

Also, psychologic stress induces the production of proinflammatory cytokines, such as TNF-alpha, IL-6, and IL-10 (Maes et al. 2000). Please turn to the protocol Cancer: Gene Therapies, Stem Cells, Telomeres, and Cytokines for a full discussion regarding proinflammatory cytokine's role in malignancies.

The Journal of the National Cancer Institute reported the effect of chronic stress on the immune system of 116 recently treated breast cancer patients. The researchers found (reproducibly) that stress levels significantly predicted (1) lower NK cell activity, (2) diminished response of NK cells to interferon-gamma, and (3) decreased proliferation of lymphocytes, white blood cells considered the army of the immune system (Andersen et al. 1998b). Oncologists often suggest stress management, such as meditation, yoga and breathing exercises, guided imagery, or spirituality, to calm the inner tempest.

Because the cells responsible for cancer surveillance work best in an environment favoring confidence and calm, it is important that the message springing from our thoughts and transmitted to cells is commensurate with healing. Fright, pessimism, and melancholy send uncertain instructions and the cells respond with a feeble effort. The enduring message (fear or assurance, despair or hopefulness, laughter or tears) reflects our hour-to-hour psyche and sets the tone for health victories or failures. Expect little more from your body than the quality of your thoughts at this very moment: "As a man thinks in his heart, so is he" (Proverbs 23:7).


Summary

The drugs, hormones, and nutrients discussed in this protocol have documented mechanisms of action that may benefit the cancer patient. The objective of implementing an adjuvant regimen consisting of multiple agents is to increase the odds of achieving a long remission. Once a remission is achieved, preventing recurrence and secondary cancers becomes a lifetime commitment.

Few oncologists aggressively seek to prevent recurrence once the primary disease appears to have been eradicated. However, the regrettable facts are that colonies of cancer cells can remain dormant in the body for years or decades before reappearing as full-blown disease that is highly resistant to treatment. This has been documented in autopsy studies of people who died of diseases other than cancer but nontheless showed significant residual metastatic tumors in their bodies.

Nutrient ......................Preventive Dose ..........Cancer Adjuvant Dose
Super Alpha-Lipoic Acid w/Biotin.250-500 mg/day....500-1000 mg/day
Coenzyme Q1030-300 mg/day Up to 400 mg/day
EPA-DHA fatty acids 1400 mg/day 2000-4000 mg/day
Garlic (PureGar Caps) or 900 mg/day Up to 7200 mg/day
Kyolic Aged Garlic (1000 mg) 1 caplet daily 3 caplets daily
Green Tea (350 mg) 1-2 caps/day 5 capsules 3 times/day
Life Extension Mix* 1 tbsp of powder, 9 tabs, or 14 capsules daily
or 14 capsules daily
1 tbsp of powder, 9 tabs,
or 14 capsules daily
Liquid Emulsified Vitamin AUp to 35,000 IU/day** Up to 100,000 IU/day**
Vitamin C (included in LE Mix)6-12 grams/day

Vitamin D3 Up to 1400 IU/day 800-4000 IU/day**
Gamma Tocopherol/Tocotrienol Formula 1 capsule/day 2-4 capsules/day
Grape Seed Extract 100 mg/day 300 mg/day
Phyto-Food (cruciferous vegetable concentrate)1 tbsp/day 1-4 tbsp/day
Melatonin 300 mcg-6 mg/day 3-50 mg/day
Selenium (included in LE Mix)200-400 mcg/day 200-400 mcg/day
Silibinin 260 mg/day Up to 2000 mg/day
Curcumin 900 mg/day 2700 mg 3 times/day
GLA (gamma-linolenic acid) 900 mg/day 900 mg/day
*Those individuals using the Life Extension Mix (powder, tablets, or capsules) are receiving a storehouse of nutrients targeted at maintaining good health. Very few of the cornerstone nutrients are not contained in the Life Extension Mix Formula, but exceptions are alpha-lipoic acid, coenzyme Q10, essential fatty acids, garlic, and melatonin. If indicated, the reader may wish to emphasize these nutrients for maximum support. Some people bolster their nutritional program by incorporating the Life Extension Booster (complete with gamma E tocopherol) in union with the Life Extension Mix. These formulas are popular from both financial and convenience perspectives. While individuals with cancer will benefit from these suggestions, a more comprehensive program is recommended, such as supplements with precise anticancer mechanisms, targeted at specific cancer cell lines or established weaknesses.
**Refer to safety precautions that appear in this protocol when taking high doses of vitamins A and D.

In too many cases, a breast, melanoma, or other cancer reemerges that was supposed to have been cured long ago. Scientists speculate that the body has natural anticancer control mechanisms that may diminish with age and exposure to physical and emotional stress factors. It is thus important for cancer patients to be vigilant in maintaining an inhospitable environment for cancer cells to propagate and protecting against age-associated immune dysfunction.

We have prepared the following chart to summarize recommendations on the basic dietary supplements and suggested doses for cancer prevention and adjuvant treatment:

In addition to the agents listed in this chart, a number of other potential adjuvant approaches are discussed in this protocol. For long-term control of cancer, some cancer patients attempt to incorporate as many of these adjuvant approaches as are tolerable and affordable. Others pick and choose which drugs, hormones, and supplements they want to consume over the long term.

Patients should read the other cancer protocols in this book, with special attention given to Cancer: Should Patients Take Dietary Supplements? and Cancer Treatment: The Critical Factors. If surgery, radiation, or chemotherapy is being considered, please refer to these specific protocols: Cancer Surgery, Cancer Radiation, and Cancer Chemotherapy.

Note: While it would be wholly inappropriate for the Life Extension Foundation to steer individuals in decisions of omission or commission regarding therapies, it would be equally improper to shun responsibility. Because we are challenged by a professional and moral commitment to assist in overcoming appalling statistics, we have discussed some controversial issues in this protocol. We look forward to new findings to better substantiate optimal therapeutic approaches.

Cancer Adjuvant Therapy Pg (1) (2) (3) (4) (5) (6) (7)

 

 

 

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