Cancer
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Cancer
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Following is an interesting study which shows a couple things. First, seafood consumption and shellfish in particular, is a protector against thyroid cancer. My guess is that this is the result of getting more ultratrace minerals. Of greater interest is the fact that long-term use of multivitamins increases thyroid cancer risk. I suspect that this is due to the depletion of trace minerals by zinc, iron, and other normal metals found in these supplements. I am working on a hypothesis that the trace mineral that is depleted that is most important in thyroid cancer is cadmium. Cadmium seems to be important in immune system function for killing tumor cells.
Lifestyle and other risk factors for thyroid cancer in Los Angeles County females. Mack WJ, Preston-Martin S, Bernstein L, Qian D. University of Southern California, Department of Preventive Medicine, Los Angeles, CA 90089, USA. PURPOSE AND METHODS: We conducted a population-based case-control study of thyroid cancer. Cases were 292 women, aged 15-54 when diagnosed between the years 1980 and 1983 (145 diagnosed in 1980-81 and 147 diagnosed in 1982-83). Female neighborhood controls (n = 292) were matched to each case on birth-year and race. RESULTS: Among women < 35 years, thyroid disease in first-degree relatives increased thyroid cancer risk [odds ratio (OR) = 2.0, 95% confidence interval (CI) = 1.1-3.7]. Risk was not associated with fish consumption, although high childhood consumption of shellfish decreased thyroid cancer risk (OR = 0.2, 95% CI = 0.05-0.7 for consumption at least a few times weekly). Among papillary thyroid cancers (82% of cases), frequent adult consumption of saltwater fish decreased risk. Cancer risk was reduced with consumption of certain vegetables, wine, and tea. Other dietary variables, including milk, beer and hard liquor, and coffee were not related to thyroid cancer risk. Among the papillary sample, risk increased with longer use of multivitamins (OR = 2.9, 95% CI = 1.2-7.4 for > 10 years of use). Smoking and body mass were not associated with thyroid cancer risk. CONCLUSIONS: These results suggest a role of family history of thyroid disease and certain dietary variables in the etiology of thyroid cancer in adult females.
Iodine and thyroid cancer risk among women in a multiethnic population: the Bay Area Thyroid Cancer Study. Horn-Ross PL, Morris JS, Lee M, West DW, Whittemore AS, McDougall IR, Nowels K, Stewart SL, Spate VL, Shiau AC, Krone MR. Northern California Cancer Center, Union City, California 94587, USA. phornros@nccc.org Research on the relationship between iodine exposure and thyroid cancer risk is limited, and the findings are inconclusive. In most studies, fish/shellfish consumption has been used as a proxy measure of iodine exposure. The present study extends this research by quantifying dietary iodine exposure as well as incorporating a biomarker of long-term (1 year) exposure, i.e., from toenail clippings. This study is conducted in a multiethnic population with a wide variation in thyroid cancer incidence rates and substantial diversity in exposure. Women, ages 20-74, residing in the San Francisco Bay Area and diagnosed with thyroid cancer between 1995 and 1998 (1992-1998 for Asian women) were compared with women selected from the general population via random digit dialing. Interviews were conducted in six languages with 608 cases and 558 controls. The established risk factors for thyroid cancer were found to increase risk in this population: radiation to the head/neck [odds ratio (OR), 2.3; 95% confidence interval (CI), 0.97-5.5]; history of goiter/nodules (OR, 3.7; 95% CI, 2.5-5.6); and a family history of proliferative thyroid disease (OR, 2.5; 95% CI, 1.6-3.8). Contrary to our hypothesis, increased dietary iodine, most likely related to the use of multivitamin pills, was associated with a reduced risk of papillary thyroid cancer. This risk reduction was observed in "low-risk" women (i.e., women without any of the three established risk factors noted above; OR, 0.53; 95% CI, 0.33-0.85) but not in "high-risk" women, among whom a slight elevation in risk was seen (OR, 1.4; 95% CI, 0.56-3.4). However, no association with risk was observed in either group when the biomarker of exposure was evaluated. In addition, no ethnic differences in risk were observed. The authors conclude that iodine exposure appears to have, at most, a weak effect on the risk of papillary thyroid cancer.
Title Groups of 6-wk-old male F344/NCr rats received a single i.v. injection of either vehicle or N-nitrosomethylurea (Cas: 684-93-5) (MNU) at a dose of 41.2 mg/kg body weight. Two wk later, groups of rats were placed on iodine-deficient, iodine-adequate, or commercial (Wayne Lab Blox) diets, or one of these diets and without previous MNU injection. Animals were sacrificed at either 52 or 77 wk, or when they became moribund. Carcinogen-treated rats on the iodine-deficient diet for up to 52 wk had significantly increased thyroid gland weights and increased incidences of both thyroid follicular cell carcinoma (90%) and diffuse pituitary thyrotroph hyperplasia (90%) at 52 wk. The majority of the follicular carcinomas were transplantable and invasive into the mammary fat pad of weanling F344/NCr rats. No other tumors induced by MNU were affected by the iodine-deficient diets. Rats fed the iodine-deficient diet without MNU injection had a 40% incidence of thyroid follicular adenomas at 52 wk and 60% at 77 wk, and a 10% incidence of follicular carcinomas at 77 wk. Thus this experiment provided evidence that the iodine-deficient diet is a potent promoter of thyroid tumors initiated by MNU and carcinogenic by itself. In addition, pituitary tumors were found in 29 of the 58 rats treated with the carcinogen alone, compared to only 3 of the 20 rats in the control groups. The vast majority of these pituitary tumors contained prolactin that was demonstrable by the avidin:biotin:peroxidase complex immunocytochemical technique.
Nutritional factors in human cancers. Giovannucci E Channing Laboratory, Department of Medicine, Brigham and Women's Hospital, Boston, Massachusetts 02115, USA. A variety of external factors interacting with genetic susceptibility influence the carcinogenesis process. External factors including oxidative compounds, electrophilic agents, and chronic infections may enhance genetic damage. In addition, various hormonal factors which influence growth and differentiation are critically important in the carcinogenic process. Diet and nutrition can influence these processes directly in the gastrointestinal tract by providing bioactive compounds to specific tissues via the circulatory system, or by modulating hormone levels. Differences in certain dietary patterns among populations explain a substantial proportion of cancers of the colon, prostate and breast. These malignancies are largely influenced by a combination of factors related to diet and nutrition. Their causes are multifactorial and complex, but a major influence is the widespread availability of energy-dense, highly processed and refined foods that are also deplete in fiber. These dietary patterns in combination with physical inactivity contribute to obesity and metabolic consequences such as increased levels of IGF-1, insulin, estrogen, and possibly testosterone. These hormones tend to promote cellular growth. For prostate cancer, epidemiologic studies consistently show a positive association with high consumption of milk, dairy products, and meats. These dietary factors tend to decrease 1.25(OH)2 vitamin D, a cell differentiator, and low levels of this hormone may enhance prostate carcinogenesis. While the nutritional modulation of growth-enhancing and differentiating hormones is likely to contribute to the high prevalence of breast, colorectal, prostate, and several other cancers in the Western world, these cancers are relatively rare in less economically developed countries, where malignancies of the upper gastrointestinal tract are quite common. The major causes of upper gastrointestinal tract cancers are likely related to various food practices or preservation methods other than refrigeration, which increase mucosal exposure to irritants or carcinogens. J Epidemiol 1996 Sep;6(3):140-7Risk factors of thyroid cancer among women in Tokai, Japan.Takezaki T, Hirose K, Inoue M, Hamajima N, Kuroishi T, Nakamura S, Koshikawa T, Matsuura H, Tajima KDivision of Epidemiology, Aichi Cancer Center Research Institute, Nagoya, Japan. To analyze the risk factors of thyroid cancer among Japanese women who generally consume much more iodine than Europeans, we conducted a hospital-based case-referent study at Aichi Cancer Center Hospital (ACCH) in Nagoya, Japan. Ninety-four female patients aged between 20-79 years with papillary or follicular carcinoma of the thyroid, and 22,666 female outpatients without cancer were used. Past history of benign thyroid mass or goiter (odds ratio: OR = 13.9) and hyperthyroidism (OR = 5.0) showed increased ORs of thyroid cancer. Thyroid cancer cases consumed coffee less frequently (OR = 0.5) and had had more experience of delivery than referents (> or = 3 times; OR = 2.5). Western style breakfast (OR = 0.5) also decreased the OR. For the multivariate analysis, past history of thyroid diseases (OR = 4.3) was positively associated with the risk of thyroid cancer and everyday coffee consumption (OR = 0.6) tended to decrease the risk. These results suggest that thyroid hormone-related factors may be involved in the risk of thyroid cancer in Japan, too. To clarify the risk involved in Japanese food, another comparative study including detailed information on iodine intake between countries and individuals is required. PMID: 8952218, UI: 97109983 Soy, tea, and cancer benefits Soy-rich diets appear to help fight certain cancers. Tea drinking has been linked to similar benefits. Two studies now find that the combo offers a potent double whammy against cancer of the breast and prostate-at least in mice. Jin-Rong Zhou and his colleagues at Harvard Medical School in Boston injected a million breast cancer or prostate cancer cells into mice engineered to possess weak immune systems. Two weeks earlier, they had replaced the drinking water of some animals with green or black tea. Others received chow laced with isoflavones, soy's biologically active antioxidants. Two groups of mice got both the mix of isoflavones and one or the other tea. Some just ate their normal diet. Two months after implantation of the cancer cells, the researchers surveyed for tumors and found that all the experimental diets had conferred some benefit. Compared with animals on the normal diet, mice given isoflavones or tea had 25 to 50 percent fewer tumors, and their tumors weighed 15 to 25 percent less. However, benefits from pairing tea and isoflavones equaled or exceeded the sum of either alone--a reduction of between 72 and 87.5 percent in tumor number and a similarly large decrease in each tumor's size. -JR. Hormones And Breast Cancer Women With Thyroid Cancer at Increased Risk for
Breast Cancer The following study may offer some clues about the nutrient relationships that lead to breast cancer. However, it will probably take time to see how this fits in with other information.
Association between malignant tumors of the thyroid gland and exposure to environmental protective and risk factors. Frentzel-Beyme R, Helmert U. Department for Environmental and Occupational Epidemiology, Bremen Institute for Prevention Research and Social Medicine, Germany. beyme@bips.uni-bremen.de Risk factors for thyroid carcinomas and adenomas were investigated using a standard questionnaire in a case-control study in Southwestern Germany, a known iodine deficiency area. A clinical registry, set up after the Chernobyl accident at the University hospital Mannheim, served as the basis for 174 incident cases of each diagnostic group. Interview data were compared within and with prevalences from a population-based matched control group of equal size from the entire area. The protective role of coffee drinking and the consumption of cruciferous vegetables, such as broccoli, were confirmed for both genders. A high consumption of tomatoes (> 200/year) was associated with an elevated risk of > 2.5 for malignant tumors but not for benign tumors in both genders. In both genders, both treatment for goiter (hyperthyroidism) and decaffeinated coffee consumption were associated with an increased risk for malignant tumors, but less so for adenomas. In women, early menarche (< 13 years) and stillbirth after first pregnancy, as well as hysterectomy, were substantial risk factors. Occupational variables and radiation, including medical indications and mammography, did not reveal particular risks. We did not address the role of regular iodine substitution, but did analyze the consumption of freshwater fish and seafood. Multivariate analyses of the most prominent risk factors confirmed the persistence of tomato consumption as a risk factor. In view of experimental evidence on the carcinogenicity of organophosphates and the neurotoxicant effect of certain agrochemicals on neuroendocrinologically regulated organs, we postulate that in Germany, importing off-season tomatoes from areas with a known history of possible inexperienced use of agrochemicals may be associated with a promoting effect for malignant neoplasias of the thyroid gland in terms of promoting already existent proliferating tissue growth.
Role of iodine in evolution and carcinogenesis of thyroid, breast and stomach. Venturi S, Donati FM, Venturi A, Venturi M, Grossi L, Guidi A. Servizio di Igiene, Regione Marche, 1-61016-Pennabilli, Italy. venturis@nf.infotel.it. The authors have hypothesized that dietary iodine (deficiency or excess) is associated with the development of some gastric and mammary cancers, as it is well-known for thyroid cancer. They report a short review of their own work and of the general literature on this correlation and on the antioxidant function of iodide in stomach, breast and thyroid. Thyroid cells phylogenetically derived from primitive iodide-concentrating gastroenteric cells which, during evolution, migrated and specialized in uptake and storage of iodine, also in order to adapt the organisms from iodine-rich sea to iodine-deficient land. Mammary cells also derived from primitive iodide-concentrating ectoderm. Stomach, breast and thyroid share an important iodide-concentrating ability and an efficient peroxidase activity, which transfers electrons from iodides to the oxygen of hydrogen peroxide and so protects the cells from damage caused by lipid peroxidation. The authors suggest that iodide might have an ancestral antioxidant function in all iodide-concentrating cells from primitive Algae to more recent Vertebrates. In Italy, gastric cancer is more frequent in farmers and in iodine-deficient populations, living in mountainous and hilly areas, than in fishermen. In the last two decades, Italian decrease of gastric cancer seems to be correlated more to the higher dietary consumption of iodine-rich fish rather than to consumption of fruit and vegetables, which indeed has decreased in Italy.
The changing incidence and spectrum of thyroid carcinoma in Tasmania (1978-1998) during a transition from iodine sufficiency to iodine deficiency. Burgess JR, Dwyer T, McArdle K, Tucker P, Shugg D. Department of Diabetes and Endocrine Services, Royal Hobart Hospital, Australia. jburges@postoffice.utas.edu.au Exposure to ionizing radiation, changing levels of iodine nutrition, and increased pathologic diagnosis of clinically unimportant thyroid neoplasia have all been proposed as explanations for a worldwide rise in the incidence of thyroid carcinoma (TC) over the past 6 decades. Tasmania is geographically an area of endemic iodine deficiency. In this report, we describe the spectrum of TC in a population averaging 450,000 persons during a 21-yr period that spans the communities transition from iodine sufficiency to iodine deficiency after discontinuation of universal iodine prophylaxis in the mid 1980s. The Tasmanian Cancer Register was used to ascertain all cases of TC diagnosed in Tasmania between 1978 and 1998. Histopathological and demographic data were reviewed. A total of 289 cases of TC were identified. Papillary TC (PTC), follicular TC, medullary TC, and other species accounted for 62%, 23%, 4%, and 11% of cases, respectively. The age standardized incidence rate for total TC increased from 2.45 to 5.33 per 100,000 for females and 0.75 to 1.76 per 100,000 for males between 1978 and 1984 and 1992 and 1998, respectively. A rise in the incidence of PTC by 4.5-fold (P < 0.05) in females and 2.1-fold in males (not significant) was the dominant change over this period. In parallel, the proportion of follicular TC relative to PTC fell from 0.35 to 0.17 during these years (P < 0.05). The rise in PTC incidence was, in part, due to an increase in the occurrence of tumors 1cm or less in diameter. Nonetheless, a 3-fold rise in incidence of larger lesions was also observed during the study period. Forty-three (24%) PTC cases had multifocal disease, 17 (40%) of whom had bilateral tumors. Familial (autosomal dominant) PTC was identified in nine (5%) total PTC cases. Prior studies have linked iodine prophylaxis to a rise in the proportion of differentiated TC, particularly PTC. Our data suggest a complex relationship between iodine nutrition and thyroid tumorigenesis. Factors such as a long latency between changes in iodine nutrition and thyroid tumorigenesis, a dose threshold for the effect of iodine nutrition on thyroid tumorigenesis, and an interaction between iodine nutrition and thyroidal sensitivity to ionizing radiation may all play a role. PROSTATE CANCER Email from the wife of a man with prostate cancer: Yesterday we went to Lahey Clinic and my husband had all kinds of tests.
They said John: Hormone Replacement Therapy Linked to Breast CancerAdding to evidence that hormone replacement therapy (HRT) can potentially raise a woman's risk of breast cancer, a new US study links recent, long-term HRT with a heightened risk of the disease. Researchers found that HRT with estrogen alone or estrogen-plus-progestin was associated with a 70% increase in breast cancer risk when the therapy was taken for 5 years within the 6 years preceding the cancer diagnosis. The findings build on previous research showing a link between long-term HRT and breast cancer and help clear up the question of whether combination HRT and estrogen-only HRT carry similar risks. In addition, the study of about 1,300 women found that HRT use had a particular link to lobular breast cancer, the form of the disease that begins in the breast's lobules. It is far less common than ductal breast cancer, which begins in the milk ducts. Women who were recent, long-time users of HRT faced a three-fold risk of lobular cancer compared with women who never used HRT. These women also had about a 50% increase in the risk of ductal cancer. JAMA February 13, 2002;287:734-741
DR. MERCOLA'S COMMENT: After all these years of estrogen hype it is becoming more and more clear to traditional medicine that the benefits of estrogen don't outweigh the risks. Estrogen has long been proven to not help with heart disease nor prevent Alzheimer's. So that leaves us with osteoporosis and hot flash relief. It has been my experience that black cohosh works far more effectively for hot flash relief. So that leaves us with osteoporosis. Well, a study published less than a year ago in JAMA showed that estrogen was not helpful to prevent against hip fractures. Fortunately one can take vitamin D, K, omega three fats and plenty of vegetables and exercise to address osteoporosis. One can only logically conclude that there is no reason for a woman to take hormone replacement therapy, unless her ovaries have been removed or she is interested in getting breast cancer. It is important to make a distinction between women who have had their ovaries removed and those that have not. Those that have will likely benefit from low dose natural human estrogen replacement while those who still have ovaries will likely not.
Complexes of metals other than platinum as antitumour agents. Kopf-Maier P. Institut fur Anatomie, Freie Universitat Berlin, Germany. The earliest reports on the therapeutic use of metals or metal-containing compounds in cancer and leukemia date from the sixteenth and nineteenth centuries. They were forgotten until the 1960s, when the anti-tumour activity of the inorganic complex cis-diammine-dichloroplatinum(II) (cisplatin) was discovered. This led to the development of other types of non-organic cytostatic drugs. Cisplatin has developed into one of the most frequently used and most effective cytostatic drugs for the treatment of solid carcinomas. Numerous other metal compounds containing platinum, other platinum metals, and even non-platinum metals were then shown to be effective against tumours in man and experimental tumours in animals. These compounds comprise main-group metallic compounds of gallium, germanium, tin, and bismuth, early-transition metal complexes of titanium, vanadium, niobium, molybdenum, and rhenium, and late-transition metal complexes of ruthenium, rhodium, iridium, platinum, copper, and gold. Several platnium complexes and four non-platnium-metal antitumour agents have so far entered early clinical trials. Gallium trinitrate and spirogermanium have already passed phase II clinical studies and have shown limited cytostatic activity against certain human carcinomas and lymphomas. The two early-transition metal complexes budotitane and titanocene dichloride have just reached the end of phase I clinical trials and have been found to have an unusual pattern of organ toxicity in man. Titanocene dichloride will soon enter phase II clinical studies. Cancer nutrition information http://www.healthy.net/library/articles/quillin/technica.asp ©
1994 Patrick Quillin, Ph.D., R.D.
This
chapter is provided for the person who enjoys knowing more of the intimate
details on how nutrition interrupts the cancer process. This section is to be
considered more exemplary rather than comprehensive. If I included all the data
in this field, then this book would be unwieldy. These references provide a
scientific foothold upon which to recommend nutrition therapy in conjunction
with traditional oncology care. For more information, see:
Books: Non-Technical CANCER THERAPY, by Ralph
Moss, PhD
ADJUVANT NUTRITION IN
CANCER TREATMENT, by Patrick Quillin, PhD,RD Purpose of Using Adjuvant
|
 | preventing the formation of carcinogens |
| increasing detoxification |
| inhibiting transformed cell replication |
| controlling expression of malignancy |
| controlling differentiation processes |
| enhancing cell to cell communication |
inhibitors of covalent DNA binding
broccoli & cabbage (phenethyl
isothiocyanate)
fruits, nuts, berries, seeds, and vegetables (ellagic acid)
fruits & vegetables (flavonoids in polyphenolic acid)
inhibitors of tumor promotion
orange & yellow
fruits & vegetables (retinol)
nuts & wheat germ (vitamin E)
fruits & vegetables (vitamin C)
green, orange, & yellow fruits and vegetables (beta-carotene)
garlic & onions (organosulfur compounds, reduce the formation of
organosoluble metabolites and increase the formation of water soluble
metabolites which are easier to excrete)
curry/tumeric (curcumin)
chili peppers (capsaicin, a vanillyl alkaloid)
inducing biotransformation
cabbage, brussel sprouts,
spinach, cauliflower and broccoli (indole-3-carbinol)
seafood & garlic (selenium)
reducing the absorption of carcinogens
fruits, vegetables,
grains & nuts (fiber)
fruits & vegetables (riboflavin chlorophyllin)
Vitamin
C and beta-carotene are effective at reversing cervical dysplasia and oral
leukoplakia in humans.9
Vitamin A derivatives (retinoids) reverse bronchial metaplasia in humans.10
Combination of folate and vitamin B-12 reversed bronchial metaplasia in humans.11
Injections of vitamin E, beta-carotene, canthaxanthin (a carotenoid) and algae
extract dramatically bolstered levels of tumor necrosis factor alpha and
reversed hamster buccal pouch tumors.12
58 adults with familial adenomatous polyps (near 100% progression to cancer if
untreated) were entered into a randomized study providing high dose vitamin C
with E and high fiber, or placebo plus low fiber diet. The high fiber group
experienced a limited degree of polyp regression.13
Beta-carotene,
vitamin A, C, E reduce the risk of cancer by radiation and chemical carcinogen
exposure. Vitamins A, D, and E inhibit the expression of oncogenes.14
Calcium supplements (2000 mg/day) provided a marked suppression of rectal
proliferation in experimental but not placebo patients. Calcium seems to
markedly inhibit the early stages of colon cancer in genetically vulnerable
individuals.15
Taking vitamin supplements was protective against colo-rectal cancer in a large
Australian study.16
The former medical director of Sloan Kettering cancer hospital in New York
(Robert Good, MD, DSc) has found that many nutrients modulate immune functions
and can protect against cancer.17
An extensive book by a former National Cancer Institute oncologist, Dr. Charles
Simone, shows the potency of nutrients to prevent cancer.18
Professors at Harvard University have published considerable evidence in the
prestigious New England Journal of Medicine showing that 90% of all
cancer is environmentally caused and therefore preventable. They cite our 500%
higher incidence of breast cancer as being related to diet. They highlight fat,
selenium, vitamin A, C, E, and fiber and prime proven nutrition cancer
preventers.19
A
theory has persisted for decades that one could starve the tumor out of the
host. Unfortunately, the tumor is quite resistant to starvation. Most studies
find more harm to the host than the tumor in either selective or blanket
nutrient deficiencies.23 Protein restriction does not affect the
composition or growth rate of the tumor, but does restrict host growth rate.24
Folate deprivation allowed the tumor to grow anyway.25 In starved
animals, the tumors grew more rapidly than in fed animals, indicating the
parasitic tenacity of tumors in the host.26 In animal studies,
starving the host led to continued tumor growth and wasting of host tissue.27
Overall, the research shows that starvation provokes host wasting while tumor
growth continues unabated.28 Pure malnutrition (cachexia) is
responsible for at least 22% and up to 67% of all cancer deaths. While the
average "healthy" American is sub-clinically malnourished, the average
cancer patient is clinically malnourished. Malnutrition is extremely common in
the cancer patient.
Of the 139 lung cancer patients studied, most tested deficient in vitamin C or
scorbutic (clinical vitamin C deficiency).29
Another study of cancer patients found that 46% tested scorbutic while 76% were
below acceptable levels for serum ascorbate.30
Experts now recommend the value of nutritional supplements, especially in
patients who require prolonged TPN support.31
Interleukin-2 therapy induced malnutrition in up to 90% of 20 patients tested.
The authors recommend prophylactic nutritional supplements to stem the immune
suppression from this iatrogenic malnutrition.32
Recommended Dietary Allowances (RDA) are not designed for cancer patients.
Supplements of vitamins, minerals, and other nutrients can benefit the cancer
patients.33
Progressive weight loss is common in cancer patients and is a major source of
morbidity and mortality.34
Wasting of tissue occurs in hypermetabolic states, most commonly for injury
patients and end-stage cancer.35
Chemo and radiation therapy are sufficient stressors in themselves to induce
malnutrition.36
Up to 80% of all cancer patients have reduced levels of serum albumin (a leading
indicator of protein/calorie malnutrition).37
There is some evidence that tumors are not as flexible in using substrates other
than glucose for fuel, hence a low carbohydrate TPN formula may have
antineoplastic value.38 A recently published position paper from the
American College of Physicians basically stated that TPN had no effect on the
outcome of cancer patients.39 Unfortunately, this article selected
non-malnourished patients. TPN treats malnutrition, not cancer.40
Weight loss drastically increases the mortality rate for most types of cancer,
while also lowering the response to chemotherapy.41
TPN improves tolerance to chemotherapeutic agents and immune responses.42
Of 28 children with advanced malignant disease, 18 received TPN for 28 days with
resultant improvements in weight gain, increased serum albumin, and transferrin
with major immunological benefits. In comparing cancer patients on TPN versus
those trying to nourish themselves by oral intake of food, TPN provided major
improvements in calorie, protein, and nutrient intake but did not encourage
tumor growth.
27 malnourished cancer patients were provide TPN and had a mortality rate of
11%, while the non-TPN group had a 100% mortality rate.43
Pre-operative TPN in patients undergoing surgery for GI cancer provided general
reduction in the incidence of wound infection, pneumonia, major complications,
and mortality.44
In one study by Mullen, the patients who were the most malnourished experienced
a 33% mortality and 46% morbidity rate, while those least malnourished had a 3%
mortality rate with an 8% morbidity rate.
There is evidence that a finely tuned TPN formula can do more than just nourish
the patient with broad spectrum nutrient coverage. TPN formulas fortified with
arginine have been shown to stimulate the immune system, accelerate wound
repair, and promote tumor reduction. Modified diets with low tyrosine (2.4 mg/kg
body wt) and low phenylalanine (3.5 mg/kg body wt) were able to elevate natural
killer cell activity in 6 of 9 subjects tested.45
In 21 adults on TPN, high amino acid solution (designed for pediatric ICU) with
30% branched chain amino acids was able to provide better nitrogen balance than
the conventional 8.5% amino acid TPN formula.46
In 20 adult hospitalized patients on TPN, the mean daily needs (based on urine
and serum ascorbate levels) for vitamin C were 975 mg with the range being
350-2250 mg.47
49 patients with small cell bronchogenic carcinoma received chemotherapy with
(21 patients) or without (28 patients) TPN. Complete remission was achieved in
85% of the TPN group versus 59% of the non-TPN group.48
In an extensive study of 3,047 cancer patients through the Eastern Cooperative
Oncology Group, weight loss was an accurate predictor of poor prognosis.49
There
is a long-standing well-accepted link between elevated insulin levels and risk
of cancer.50
Cancer cells demonstrate a 3 to 5 fold increase in glucose uptake compared to
healthy cells.51
Cancer thrives on glucose while also initiating gluconeogenesis and insulin
resistance.52 Lipid based parenteral solutions for cancer patients
slow cancer growth.
Modest ingestion of glucose (75 gm) caused a measurable decline in cell-mediated
immunity in 7 healthy human volunteers. Mechanism of action is probably via
elevated insulin, which competes with mitogens for binding sites on lymphocytes.53
In animal studies, progressive increase in sucrose in the diet leads to a
dose-dependent decline in antibody production.54
Healthy human volunteers ingested 100 gram portions (average US daily intake) of
simple carbohydrates from glucose, fructose, sucrose (white sugar), honey, and
orange juice. While simple sugars signficantly impaired the capacity of
neutrophils to engulf bacteria, starch ingestion did not have this effect.55
In a study comparing 50 colorectal cancer patients to healthy matched controls,
the cancer patients ate considerably more sugar and fat than the healthy people.56
An epidemiological study of 21 countries suggests that high sugar intake is a
major risk factor toward breast cancer.57
Animals were fed isocaloric diets of carbohydrates. The group eating more sugar
developed significantly more mammary tumors than the starch-fed group.58
In an extensive review of
the literature, Dr. Adrienne Bendich found the following data on nutrient
toxicity59:
| B-6 can be used at up to 500 mg (250 times RDA) for up to 6 years
with safety. |
| Niacin (as nicotinic acid) has been recommended by the National
Institute of Health for lowering cholesterol at doses of 3000-6000 mg/day
(150-300 times RDA). Time release niacin is more suspect of causing toxicity
as liver damage. |
| Vitamin C was tested in eight published studies using double blind
placebo controlled design. At 10,000 mg/day for years, vitamin C produced no
side effects. |
| High doses of vitamin A (500,000 iu daily) can have acute reversible
effects. Teratogenecity is the most likely complication of high dose vitamin
A intake. |
| Vitamin E intake at up to 3000 mg/day for prolonged periods has been
shown safe. |
| Beta-carotene has been administered for extended periods in humans
at doses up to 180 mg (300,000 iu) with no side effects or elevated serum
vitamin A levels. |
In a separate review of the literature on nutrient toxicity by John
Hathcock, PhD, a Food and Drug Administration toxicologist, the following data
was reported60:
| Vitamin A toxicity may start as low as 25,000 iu/day (5 times RDA)
in people with impaired liver function via drugs, hepatitis, or protein
malnutrition. Otherwise, toxicity for A begins at several hundred thousand
iu/day. |
| Beta-carotene given at 180 mg/day (300,000 iu or 60 times RDA) for
extended periods produced no toxicity, but mild carotenemia (orange
pigmentation of skin). |
| Vitamin E at 300 iu/day (10 times RDA) can trigger nausea, fatigue,
and headaches in sensitive individuals. Otherwise, few side effects are seen
at up to 3,200 iu/day. |
| B-6 may induce a reversible sensory neuropathy at doses of as low as
300 mg/day in some sensitive individuals. Toxic threshold usually begins at
2000 mg for most individuals. |
| Vitamin C may induce mild and transient gastro-intestinal distress
in some sensitive individuals at doses of 1000 mg (16 times RDA). Otherwise,
toxicity is very rare at even high doses of vitamin C intake. |
| Zinc supplements at 300 mg (20 times RDA) have been found to impair
immune functions and serum lipid profile. |
| Iron intake at 100 mg/day (6 times RDA) will cause iron storage
disease in 80% of population. The "window of efficacy" on iron is
probably more narrow than with other nutrients. |
| Copper can be toxic, though dose is probably related to the ratio
with other trace minerals. |
| Selenium can be toxic at 1-5 mg/kg body weight intake. This would
equate to 65 mg/day for the average adult, which is 812 times the RDA of 80
mcg. Some sensitive individuals may develop toxicity at 1000 mcg/day. |
| Manganese can be toxic, though little specific information can be
provided for humans. |
Vitamin
C enhanced the chemotherapeutic action of levodopa methylester and increased
survival time in B16 melanoma-bearing mice.61
Niacin supplementation in animals reduced the cardiotoxicity of the drug without
inhibiting the effectiveness of the drug.62
Low serum levels of vitamin A and E were indicative of human cancer patients who
responded poorly to chemotherapy.63
50 previously untreated cancer patients randomly received radiation therapy with
or without 5 grams/day of vitamin C supplements. After 1 month, 87% of the
vitamin C treated group showed a complete response (disappearance of all known
disease) compared to 55% of the control.64
Vitamin C and K separately showed anti-tumor activity against human cancer cells
in vitro, but became synergistically effective at 2% the regular dosage when
used together.65
Vitamin C had no effect on the anti-tumor activity of adriamycin but did prolong
the life of the animals treated with adriamycin.66
B-6 deficient mice exhibited enhanced tumor susceptibility and increased tumor
size.67
22 patients with precancerous conditions, 19 patients with malignant oral
lesions and 13 healthy controls were evaluated with respect to serum selenium
levels and response to selenium therapy (300 mcg/day). Using selenium as sole
therapy, there was a 38.8% objective response rate in treated patients.68
Human prostatic cancer cells in vitro were markedly inhibited when vitamin E was
added to the adriamycin.69
Vitamin E enhanced the growth inhibitory effect of vincristine on mouse melanoma
cells.70
Vitamin E therapy (1600 iu/day) begun 5-7 days prior to therapy prevented 69% of
adriamycin patients from experiencing baldness.71 Other studies have
not always reached the same conclusion but have not followed this protocol. It
appears important to begin vitamin E therapy at least 7 days prior to
chemotherapy.
Calcium and vitamin D improved the efficacy of thioTEPA and other anti-neoplastic
drugs against Hodgkin's disease and lung cancer.72
Selenium supplements (200 mcg/day) in 23 patients with ovarian cancer or
metastatic endometrial cancer showed less host tissue damage than the untreated
group.73
A derivative of ascorbic acid (sodium benzylideneascorbate, SBA) was given in
daily dose of 200 mg/m2 to 55 patients with inoperable carcinoma. 8 patients
achieved a complete response, 21 achieved partial response, 25 remained stable,
and 1 showed progression of disease. The activity of this medication was
increased with concurrent tamoxifen use.74
While tamoxifen is the commonly used drug to inhibit estrogen-dependent tumor
growth, vitamin C has clearly demonstrated the ability to inhibit
estrogen-dependent tumor growth in hamsters.75
Vitamin E and selenium helped reduce the lipid peroxidation-induced
cardiotoxicity from adriamycin in animal models without inhibiting effectiveness
of therapy.76
Potassium bromate can cause nephrotoxicity via renal oxidative DNA damage. In
rat model, pre and post treatment with cysteine and glutathione (amino acids)
and vitamin C protected against oxidative damage in the kidneys.77
Niacin (vitamin B-3) as nicotinamide is able to dramatically improve the
response of hypoxic radioresistant tumors in animal models. Anaerobic tumors do
not respond well to radiation therapy, while niacin seems to improve aerobic
metabolism to make solid tumors more vulnerable to radiation therapy.78
Vitamin E topically applied (400 mg per lesion, twice daily for 5 days) to oral
lesions induced by chemotherapy provided substantial relief in 6 of 9 patients
while only 1 of 9 placebo treated patients had any relief from oral mucositis.
Vitamin E seemed to best help patients taking cisplatin and 5-fluorouracil. Oral
mucositis is often the beginning of anorexia which deteriorates into clinical
malnutrition.79
In mouse and guinea pig models, vitamin C prolonged the life of animals treated
with adriamycin without affecting the anti-tumor activity of this drug. Vitamin
C was able to prevent the adriamycin-induced cardiomyopathy as determined by
electron microscopy.80
While tamoxifen is a drug that binds up circulating estrogen, which can incite
tumor growth, studies show that wheat fiber does the same thing while also
reducing secondary bile acids and bacterial enzymes associated withcolon
cancer--without the potential carcinogenic effects of tamoxifen.81
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Many nutrients taken orally can provide pharmacological changes in immune
function in humans. Protein, arginine, glutamine, omega-6 and omega-3 fats,
iron, zinc, vitamins E, C, and A have all been proven to modulate immune
functions.82
Vitamin A deficiency causes reduced lymphocyte response to antigens and mitogens,
while beta-carotene supplements stimulate immune responses.83
There is extensive literature supporting the importance of vitamin B-6 on the
immune system. In one study, B-6 supplements (50 mg/day) provided a measurable
improvement in immune functions (T3 and T4 lymphocytes) for 11 healthy well fed
older adults.84
Various B vitamins have been linked to the proper functioning of antibody
response and cellular immunity.
Folate deficiency decreases mitogenesis.
Deficiency of vitamin C impairs phagocyte functions and cellular immunity.
Vitamin E deficiency decreases antibody response to T-dependent antigens, all of
which gets worse with the addition of a selenium deficiency. In test animals,
normal vitamin E intake was not adequate to optimize immune functions.85
Modest supplements of vitamin E have been shown to enhance the immune response.
While iron deficiency can blunt immune functions, iron excess can increase the
risk for cancer.86
Zinc exerts a major influence on the immune system. Lymphocyte function is
seriously depressed and lymphoid tissues undergo general atrophy in
zinc-deficient individuals. The lymphocytes in zinc-deficient animals quickly
lose their killing abilities (cytotoxicity) and engulfing talents (phagocytosis)
for tumor cells and bacteria. Natural killer cell and neutrophil activity is
also reduced. All of these compromised immune activities elevate the risk for
cancer.
Copper plays a key role in the production of superoxide dismutase and cytochrome
systems in the mitochondria. Hence, a deficiency of copper is manifested in a
depressed immune system, specifically reduced microbicidal activity of
granulocytes.
Selenium works in conjunction with vitamin E to shield host cells from lipid
peroxidation. Humoral immune response is depressed in selenium deficient
animals. Selenium and vitamin E deficiencies lead to increased incidence of
enteric lesions. Lymphocyte proliferation is reduced in selenium deficiency. The
theory is that selenium and vitamin E help to provide the host immune cells with
some type of "bullet proof plating" against the toxins used on foreign
cells. Hence, one immune body can live on to destroy many invaders if enough
vitamin E and selenium allow for these critical chemical shields.
In magnesium deficiency, all immunoglobulins (except IgE) are reduced, along
with the number of antibody forming cells. Magnesium is crucial for lymphocyte
growth (involvement in protein metabolism) and transformation in response to
mitogens. Prolonged magnesium deficiency in animals leads to the development of
lymphomas and leukemia.
Iodine plays an important role in the microbicidal activity of polymorphonuclear
leukocytes. Activated neutrophils may use the conversion of iodide to iodine to
generate free radicals for killing foreign invaders.
Boron is an interesting trace mineral, since it is now recognized for its role
in preventing osteoporosis, yet is still not considered an essential mineral.
Boron deficiency in chicks creates immune abnormalities like arthritis.
Toxic trace minerals, like cadmium, arsenic and lead all blunt the immune
system.
The quality and quantity of fat in the diet plays a major role in dictating the
health of the immune system. A deficiency of the essential fatty acid (linoleic
acid) will lead to atrophy of lymphoid tissue and a depressed antibody response.
And yet excess intake of polyunsaturated fatty acids will also diminish T-cell
immune responsiveness. Since fat directly affects prostaglandin pathways, and
prostaglandins (depending on the pathway) can either depress or enhance immune
function, fat intake is crucial in encouraging a healthy immune system. Oxidized
cholesterol is highly immuno-suppressive. Cholesterol is less likely to oxidize
while in the presence of anti-oxidants, like vitamin E, C, and beta-carotene.
Basically, nutrition plays a key role in the effectiveness of the immune system.
Primary assessment techniques to find the relative nutrient status of the immune
system include:
| Clinical: dietary intake, physical examination |
| Anthropometric: skin fold thickness, percent body fat |
| Hematologic: hemoglobin and ferritin levels |
| Biochemical: serum albumin, serum transferrin, creatinine/height
index, zinc status |
| Immunologic: lymphocyte count, terminal transferase activity,
T-cells |
| Miscellaneous: hand grip strength, dark adaptation, taste acuity |
A main goal of this nutrition program is to optimize the functioning of the
immune system via foods and nutritional supplementation (pills, powder, or TPN).
A healthy immune system is better able to join in the battle to rid the body of
tumor cells.
VITAMINS
Vitamin E.
Was used (via injections) to reverse oral tumor progress in animals with induced
tumors.89
Prevents and may even reverse tumor growth in animals with chemically induced
tumors.90
Was able to prevent expected tumors in lab animals exposed to DMBA.91
Increased the effectiveness and specific toxicity of chemotherapy agents on
tumors in culture.92
Relieves most cystic breast disease, which indicates that E can treat
pre-cancerous conditions.93
May be anti-neoplastic by virtue of its ability to protect the prostaglandin
prostacyclin.94
Protects against damage from radiation therapy.95
In combination with selenium was able to prevent expected tumors in animals
after DMBA injections.
Significantly elevated the microsomal hydroperoxidase activity.96
And selenium provided partial protection against cardiotoxicity in adriamycin
use on rabbits. Best protection was aforded by high dose vitamin E.97
Deficiency accentuated the cardiotoxicity of adriamycin in rats.98
Increased (in vitro) the therapeutic benefits of chemotherapy agents on human
prostate cancer cells.99
Directly stunted the growth of mouse melanoma cells in vitro.100
Topical application of DMSO and vitamin E produced a 68% decrease in skin
necrosis on mice given adriamycin.101
Mice with oral cancer were supplemented with injections of vitamin E,
beta-carotene, canthaxanthin, and algae extract. Major improvements in tumor
necrosis factor were measured in the supplemented mice, who also experienced
varying levels of tumor regression.102
Reduced the cardiotoxic effects of daunomycin (similar to adriamycin) in test
animals.103
And vitamin K3 (menadione) enhanced the anti-metabolic activity of the
chemotherapy agents 5FU and leucovorin in vitro.104
Sensitized tumor cells, but not healthy cells, to radiation therapy for enhanced
effectiveness.105
Use in radiation therapy reduces toxic side effects.106
Patients with peripheral neuropathy (common as a side effect for certain chemo
agen
