The good news is that many of the 4 million people being treated for cancer in America will survive the disease and go on to live full and productive lives.
While the numbers that survive are far too low (about 44%), many of the more than 1500 daily cancer deaths occur because patients and their families are unaware of the depth of the resources currently available. Unfortunately, some die avowing they would never resort to natural medicine, while others are interested but lack the expertise to implement the program to their best advantage. Regrettably, some turn to alternative care fairly late in the course of the disease process, weakening the probability of recovery.
Mainstream medicine (relying upon surgery, chemotherapy, and radiation) may initially appear successful, but the indications of the disease process are less often addressed. Conventional cancer treatments are not for those individuals who are frail in body or spirit. For the past 30 years, cancer therapies have experienced tremendous setbacks because of an associated toxic response, resulting in significant numbers of treatment-induced deaths rather than disease-induced fatalities. Awareness regarding historic numbers of unsuccessful outcomes has forced patients to look for alternatives to bolster survival odds. Many who use alternative therapies report doing so without their oncologist's knowledge, fearful of criticism or rejection by a physician (Richardson et al. 2000).
The University of Texas M.D. Anderson Cancer Center (Houston) found that 99.3% of patients had heard of complementary medicine, and 68.7% of patients reported having used at least one unconventional therapy (Richardson et al. 2000). About 75% of the patients surveyed, however, yearned for more information concerning complementary medicine and about one-half of those participating in the survey wanted the information to come from their physician.
Until most recently, major medical schools granted only a few hours to nutritional education out of the hundreds of academic hours required to complete medical school. The exclusion began when Abraham Flexner (commissioned to correct inequities occurring in medical schools) penned the Flexner Report of 1910. His contribution, entitled Medical Education in the United States and Canada, closed smaller medical schools and forced those that survived to adopt a uniform curriculum that excluded nutritional courses. Thus, some physicians emerged from medical schools, scoffing at the concept of nutrition influencing health or overcoming disease.
Sir William Osler (1849-1919), chief physician at Johns Hopkins's School of Medicine, drilled into students that medical research must be validated and replicated to be good medicine. This led to controlled experiments (as randomized, controlled trials) that became the backbone of mainstream medicine. Nutritional protocols often used multiple nutrients, a difficult model to apply in clinical trials. Testing a single nutraceutical denied the patient full support of nutritional pharmacology, an injustice when treating a seriously ill patient. In addition, trials are expensive to conduct and early natural healers (by and large) did not represent an affluent subset of society.
But, ever so slowly, the medical scene is being revolutionized. According to the American College for Advancement in Medicine, physicians (in many cases) are showing eagerness to learn more about natural medicine and how to best implement it into their practice (Corbin-Winslow et al. 2002). Scientists, teaching at nutritional seminars, report attendees are often medical doctors, a vast departure from years past.
PREVENTING AND CONTROLLING CANCER
While some individuals will be reading this protocol looking for help managing a malignancy, others will be focusing upon prevention and recurrence. The alphabetical list that follows provides quick guidelines for structuring a program, highlighting major nutrients in the prevention and treatment of cancer.
These recommendations should not be implemented individually in aggressive cancers without careful consultation of the remainder of the material. Cancer patients (and physicians) should be deliberate about reading the entirety of this protocol in order to avoid missing information that could prove to be lifesaving. Note: It is important that the reader also consult the protocols entitled Cancer Treatment: The Critical Factors and Cancer: Should Patients Take Dietary Supplements
The dosages required for treating cancer (which are considerably larger than those required for prevention) can change the effects that a nutrient has on the body. The risk is multidirectional. Overdosing or underdosing, as well as a lack of patient awareness regarding the full potential of natural pharmaceuticals, hampers recovery.
THE CRITICAL IMPORTANCE OF SCHEDULED BLOOD TESTS
It is important to measure the successes or losses in regard to treatment-associated tumor response. Evaluating tumor markers in the blood or tumor imagery provides a basis for calculating regression of the disease. In addition, tumor markers provide direction for introducing other therapies if failures are evidenced.
Table 1: Type of Cancers and the Tumor Marker Used for Assessment
Type of Cancer Tumor Marker Blood Test
Ovarian cancer CA 125, CK-BB
Prostate cancer PSA, PAP, prolactin, testosterone
Breast cancer CA 27.29, CEA, alkaline phosphatase, and prolactin (or CA 15-3 rather than the CA 27.29)
Colon, rectum, liver, stomach, and other organ cancers CEA, CA 19-9, AFP, TPS, and GGTP
Pancreatic cancer CA 19.9, CEA, and GGTP
Leukemia, lymphoma, and Hodgkin's disease LDH, CBC with differential, immune cell differentiation and leukemia profile
It is also important to evaluate the effectiveness of immune-boosting therapies and guard against anemia and therapeutic toxicities. At a minimum, a monthly complete blood chemistry (CBC) test that includes assessment of hematocrit, hemoglobin, and liver and kidney function should be done in all cancer patients undergoing treatment.
An immune cell test should be performed bimonthly, measuring total blood count, CD4 (T-helper), CD4/CD8 (T-helper-to-T-suppressor) ratio, and NK (natural killer) cell activity. Also consider tests measuring cortisol levels (Cortisol am and pm) and HCG (human chorionic gonadotropin), a hormone that may be elevated 10-12 years prior to a diagnosis of cancer. For information regarding test availability call (800) 208-3444.
COMPLEMENTARY THERAPIES
When describing the various complementary cancer therapies, it is not possible to endorse one supplement, hormone, or drug over another. We have provided as much evidence as space allows so that patients and their physicians can evaluate what approach may be suited for the individual situation.
A great deal of effort has been made to identify therapies that are substantiated in published scientific literature or that provide a cancer patient with the opportunity to experiment with cutting-edge treatment strategies. The focus of our effort has been to identify potentially lifesaving therapies that have been overlooked by mainstream oncology. We also attempt to discuss both positive and negative studies when applicable.
The Life Extension Foundation can assume no responsibility for outcome, apart from a self-assigned duty to stay abreast of the most promising of therapies and to share the data with members. No warranties (expressed or implied) accompany the material; neither is the information intended to replace medical advice. As always, each reader is urged to consult professional help for medical problems, especially those involving cancer. All supplements, drugs, and hormones are listed alphabetically and not in order of importance.
Alpha-Lipoic Acid--is a powerful antioxidant that regulates gene expression and preserves hearing during cisplatin therapy
Lester Packer, Ph.D. (scientist and professor at the Berkeley Laboratory of the University of California), refers to lipoic acid as the most powerful of all the antioxidants; in fact, Packer says that if he were to invent an ideal antioxidant, it would closely resemble lipoic acid (Packer et al. 1999). Alpha-lipoic acid claims anticarcinogenic credits because it independently scavenges free radicals, including the hydroxyl radical (a free radical involved in all stages of the cancer process and linked to an increase in the likelihood of metastasis).
Lipoic acid increases the efficacy of other antioxidants, regenerating vitamins C and E, coenzyme Q10, and glutathione for continued service. In fact, lipoic acid boosts the levels of glutathione by 30-70%, particularly in the lungs, liver, and kidney cells of laboratory animals injected with the antioxidant. In addition, glutathione tempers the synthesis of damaging cytokines and adhesion molecules by influencing the activity of nuclear factor kappa B (NF-kB), a transcription factor (Exner et al. 2000). Note: A great deal of material relating to NF-kB is presented in the protocol Cancer Treatment: The Critical Factors.
Lipoic acid can down-regulate genes that accelerate cancer without inducing toxicity. So responsive are cancer cells that laboratory-induced cancers literally soak up lipoic acid, a saturation that increased the lifespan of rats with aggressive cancer by 25% (Karpov et al. 1977).
Alpha-lipoic acid was preferentially toxic to leukemia cells lines (Jurkat and CCRF-CEM cells). The selective toxicity of lipoic acid to Jurkat cells was credited (in part) to the antioxidant’s ability to induce apoptosis. Lipoic acid activated (by nearly 100%) an enzyme (caspase) that kills leukemia cells (Pack et al. 2002). Other researchers showed that lipoic acid acted as a potentiator, amplifying the anti-leukemic effects of vitamin D. It is speculated that lipoic acid delivers much of its advantage by inhibiting NF-kB and the appearance of damaging cytokines (Sokoloski et al. 1997; Zhang et al. 2001). Finding that lipoic acid can differentiate between normal and leukemic cells charts new courses in treatment strategies to slow or overcome the disease (Packer et al. 1999).
As with all antioxidants, the appropriateness of using lipoic acid with chemotherapy arises. Animal studies indicate that alpha-lipoic acid decreased side effects associated with cyclophosphamide and vincristine (chemotherapeutic agents) but did not hamper drug effectiveness (Berger et al. 1983). More recently, a combination of alpha-lipoic acid and doxorubicin resulted in a marginally significant increase in survival of leukemic mice (Dovinova et al. 1999). Nonetheless, the definitive answer regarding coupling antioxidants with conventional cancer therapy is complex. Factors, such as type of malignancy, as well as the nature of the cytotoxic chemical and even the time of day the agents are administered, appear to influence outcome (please consult the protocol Cancer: Should Patients Take Dietary Supplements to learn more about the advisability of antioxidant therapy during conventional treatments).
To its credit, lipoic acid appears able to counter the hearing loss and deafness that often accompanies cisplatin therapy. Depreciated hearing occurs as free radicals, produced as a result of treatment, plunder the inner ear; lipoic acid preserves glutathione levels and thus prevents deafness in rats (Rybak et al. 1999).
A suggested lipoic acid dosage for healthy individuals is from 150-300 mg a day. Degenerative diseases usually require larger dosages (sometimes as much as 500 mg 3 times a day).
Arginine
Various scientists have attempted to describe the complex role of arginine in cancer biology and treatment. L-arginine is the common substrate for two enzymes, arginase and nitric oxide synthase. Arginase converts L-arginine to L-ornithine, a pathway that can increase cell proliferation. Nitric oxide synthase converts L-arginine to nitric oxide, a conversion process with uncertain effects regarding cancer.
A positive study conducted by a team of German researchers showed that arginine contributed significantly to immune function by increasing levels of white blood cells. Scottish scientists added that dietary supplementation with arginine in breast cancer patients enhanced NK cell activity and lymphokine cytotoxicity (Brittenden et al. 1994). (Lymphokines are chemical factors produced and released by T-lymphocytes that attract macrophages to a site of infection or inflammation in preparation for attack.) Various researchers have shown that increasing arginine increases neutrophils (white blood cells that remove bacteria, cellular debris, and solid particles), significantly upgrading host defense (Muhling et al. 2002).
Apart from enhancing immune function, arginine increases a number of amino acids, creating the possibility of an amino acid imbalance. Oversupplying some amino acids while undersupplying others is thought to destabilize the tumor. All cells, both healthy and diseased, have amino acid requirements; if not met, the cell is significantly disabled (Muhling et al. 2002). Amino acid manipulation has been applied in oncology for decades with varying degrees of success.
Interesting studies have emerged regarding arginine or arginine analogs in cancer treatment. For example, infusions of arginine significantly reduced the incidence of liver and lung metastasis in laboratory mice. Earlier research found that supplemental arginine altered the number of tumor-infiltrating lymphocytes in human colorectal cancer, offering important implications for new strategies in cancer treatment (Heys et al. 1997). Though many factors are involved (including appropriate dosages), Japanese researchers found that arginine induced apoptosis in pancreatic (AR4-2J) cells, inhibiting cell proliferation (Motoo et al. 2000).
The two faces of arginine, however, cloud dosing with confidence. The role of nitric oxide (NO), a molecule synthesized from arginine, remains controversial and poorly understood. While a few reports indicate that the presence of NO in tumor cells or their microenvironment is detrimental to tumor-cell survival, and subsequently their metastatic potential, a large body of data suggests that NO actually promotes tumor progression. Illustrative of its fickleness, NO was recently identified as a downstream regulator of prolactin, an inhibitor of apoptosis. However, arginine stimulated proliferation of prolactin-dependent Nb2 lymphoma cells in laboratory rats (Dodd et al. 2000). In addition, NO production (by murine mammary adenocarcinoma cells) promoted tumorcell invasiveness. Whereas, introducing NO inhibitors resulted in an antitumor, antimetastatic profile (Orucevic et al. 1999).
Ambiguity and nonconformity reduce arginine's role at the present time to adjunctive support with either traditional cancer treatment or fish oil supplementation. A heartening report regarding arginine, fish oil, and doxorubicin therapy appears in this protocol in the section devoted to Essential Fatty Acids (Ogilvie et al. 2000). Nonetheless, the diverse biological properties of L-arginine demand further careful studies, clarifying chemopreventive advantages and endangerments (Szende et al. 2000). 
| Table 1: Type of Cancers and the Tumor Marker Used for Assessment |
| Type of Cancer |
Tumor Marker Blood Test |
| Ovarian cancer |
CA 125, CK-BB |
| Prostate cancer |
PSA, PAP, prolactin, testosterone |
| Breast cancer |
CA 27.29, CEA, alkaline phosphatase, and prolactin (or CA 15-3 rather than the CA 27.29) |
| Colon, rectum, liver, stomach, and other organ cancers |
CEA, CA 19-9, AFP, TPS, and GGTP |
| Pancreatic cancer |
CA 19.9, CEA, and GGTP |
| Leukemia, lymphoma, and Hodgkin's disease |
LDH, CBC with differential, immune cell differentiation and leukemia profile |
제 목 : ca.adjuvant tx.
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