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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 Vitamin Depot Online.com 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). |
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