The Role of Nutrition in Cancer Prevention and Treatment
Nutrition ought to be an integral part of conventional cancer care
This chapter explaining the role of nutrition in relation to cancer prevention and treatment does not rightfully belong in a book devoted to complementary approaches to cancer care; it should be part of mainstream medical care for cancer patients. Health-promoting nutrition, recognized by leading epidemiologists, oncologists, and molecular biologists alike to be a factor in reducing cancer risk by some 30-40% (WCRF 1997), should form a major part of the curriculum for medical students, should be taught to all children from primary school age, practised within our daily lives, and should form an integral part of cancer treatment for all cancer patients.
Yet perversely the opposite situation prevails. The commercial messages beamed out via the media promote the consumption of manifestly unhealthy foods high in fats, sugar, and salt, and the ‘sexy’ consumption of alcoholic, caffeinated, sugary, and carbonated beverages. Negative messages pervade the media, criticizing and ridiculing the consumption of healthy and organic foods, dietary supplements and natural remedies, while physicians and holistic centres for cancer patients recommending dietary regimens fight desperately for survival, let alone for professional legitimacy.
I didn’t always feel this stridently. Until the mid 1980s I was a molecular biology scientist working in the field of agricultural biotechnology, endeavouring to find ways to increase agricultural yields of crops such as soybeans. Since I moved from that field to explore the health-enhancing benefits of nutrition, I have written books and scientific articles, (Goodman, 1988, 1991, 1994, 1995, 1997; Goodman and Daniel 1994; Goodman et al. 1994) compiled databases relating to cancer and nutrition (BCHC 1993) as well as many aspects of complementary medicine (Positive Health).
During the past 15 years, I have witnessed the almost total marginalization of nutrition in cancer treatment, despite the existence of many thousands of high quality published research papers in the most highly respected scholarly journals attesting to the important role of nutrition in all stages of cancer aetiology and development (WCRF 1997). Furthermore, having read widely from the huge literature attesting to the massive environmental contributions to cancer (Epstein 1998), I have realized that there has also been an almost total separation of the knowledge bases of these three integrally-linked disciplines – nutritional research, environmental research, and oncology care.
It is incomprehensible to me as a research scientist, as well as a scandal to the medical profession, that nutrition does not play a central role in cancer care, given the massive body of published literature documenting the important role played by nutrition both in the prevention and the treatment of cancer (BCHC 1993; Goodman 1998; CRC 1999; WCRF 1997; Wheatley 1998).
The wider general public has become much more aware than have physicians of the role of environmental carcinogens as well as the benefits of healthful nutrition in the fight against cancer. It is my hope to attempt to activate an acute interest in nutrition among physicians by providing a flavour of the findings of this research and in directing the reader to the massive body of research within the literature sources appended.
Nutrition’s vital role in cancer prevention and treatment
The extent of the published scientific evidence regarding the role of food and nutrition in cancer prevention and treatment is considerable. The initial database compiled for the Bristol Cancer Help Centre (BCHC, 1993) consisted of 5000 records during the previous decade alone! The database compiled for Positive Health numbers some 1000 references since 1993 and the World Cancer Research Fund’s epic tome (WCRF 1997) cites more than 3000 references covering:
* patterns of diet and cancer;
* diet and the cancer process, including the genetic and molecular processes of cancer initiation, promotion, and progression;
* types of scientific evidence published;
* 18 distinct types of cancer and how they are affected by food and nutrition;
* dietary constituents, i.e. carbohydrates, energy factors, fats, proteins, alcohol, vitamins, minerals;
* foods and drinks, i.e. grains, vegetables and fruits, pulses, nuts and seeds, meat, poultry, fish, eggs, milk, coffee, tea, and other drinks;
* food preparation, including contaminants, additives, processes such as curing, salting, and other cooking methods.
The evidence is graphically illustrated with charts, colour drawings, and tables listing, in great detail, the scientific literature from which the text is drawn.
Some 15 distinguished international scientists assembled this massive amount of evidence which, in short, concluded the following with regard to cancer prevention:
* That 30%-40% of all cancers, representing the prevention of some 3-4 million cancer cases each year, could be prevented using appropriate diet, physical activity, and maintaining proper body weight;
* That diets with substantial and varied amounts of fruits and vegetables could prevent 20% or greater of all cancer cases;
* That if alcohol consumption were maintained within recommended limits, up to 20% of aerodigestive tract, colon, rectal, and breast cancer cases could be prevented;
* That appropriate diet could prevent most stomach cancers and that colon and rectal cancers are mainly preventable by diet, physical activity, and appropriate body weight.
Given the paltry attention and resources currently expended upon nutritional methods for the prevention and treatment of cancer, and considering the mammoth implications of the above projections, along with its respectable documentation of scientific literature, a great deal needs to change in order to accommodate nutritional methodologies into cancer care.
However, very few physicians can afford the luxury of reading the entire research literature for cancer, or neoplasms as it is categorized within MedLine. Hence, here are a few examples of published research from the literature illustrating the extent of progress in nutritional cancer research.
Evidence from epidemiological and clinical trials
Although there is a vast literature on nutrition and cancer, few studies addressed supplemental nutrients directly. Patterson et al. (1997) compared the results of 7 clinical trials, 16 cohort and 36 case-control studies and demonstrated the effects of nutrients which are distinguishable from the effects of biologically active compounds in foods.
Randomized clinical trials have not demonstrated significant protective effects of beta-carotene, but have found protective effects of vitamin E against prostate cancer, vitamin A, zinc, beta-carotene, vitamin E, and selenium against stomach cancer, and selenium against total, lung, and prostate cancers.
Cohort studies provide scant evidence that vitamin supplements are associated with cancer. Case-control studies have demonstrated an inverse association between vitamin C and bladder cancer, several supplemental vitamins and oral/pharyngeal cancer and vitamin E and several cancers. Inverse associations between vitamin E and colon cancer have been found by a randomized clinical trial, a cohort study, and a case-control study.
In conclusion, there is, overall, modest evidence regarding the protective effects of nutrients from supplements against a number of cancers. Future studies of vitamin supplement use and cancer are justified, however methodological problems which impede the ability to assess supplement use, and statistical modelling of the relation between cancer risk and supplement use, require ironing out.
Zhang et al. (1999) studied the associations between dietary intakes of carotenoids, vitamins A, C, and E, consumption of fruits and vegetables and breast cancer risk. The authors conducted a large, prospective study to evaluate long-term intakes of these nutrients and breast cancer risk, in a cohort of 83,234 women, aged 33-60 years in 1980, who were participants in the Nurses’ Health study. During 1994, the authors identified 2697 incident cases of invasive breast cancer (784 premenopausal; 1913 postmenopausal).
There was a weak, inverse association between intakes of beta-carotene from food and supplements, lutein/zeaxanthin and vitamin A from foods and breast cancer risk in premenopausal women. There were strong inverse associations for increasing quintiles of alpha-carotene, beta-carotene, lutein/zeaxanthin, total vitamin C from foods and total vitamin A in premenopausal women with a positive family history of breast cancer. There was also an inverse association for increasing quintile of beta-carotene in premenopausal women who consumed 15 g or more of alcohol daily. Additionally, premenopausal women consuming 5 or more servings per day of fruits and vegetables had modestly lower risk of breast cancer than women who consumed fewer than 2 servings per day (relative risk (RR) = 0.77). The latter association was stronger in premenopausal women with a positive family history of breast cancer (RR = 0.29) or those women consuming 15 g or more of alcohol per day (RR = 0.53). The authors concluded that the consumption of fruits and vegetables high in specific carotenoids and vitamins may reduce the risk of breast cancer in premenopausal women.
La-Vecchia and Decarli (1996) noted that following early increases, mortality rates from oesophageal cancer have levelled off in Italy over the past two decades and are now intermediate on a European scale: 4.7/100,000 men; 0.8/100,000 women. The authors say that this reflects trends in consumption of tobacco and alcohol, major risk factors for this type of cancer. Within Italy there is considerable variation in rates of oesophageal cancer, with high mortality areas in the North-East. The relative risk (RR) of oesophageal cancer was 4.3 in heavy smokers and 3.5 in heavy drinkers, based upon a case-control study in northern Italy. A diet poor in fresh fruit and vegetables was also related to risk (RR = 2.5).
Regarding population attributable risk, 71% of cases in men and 32% in women were accounted for by tobacco smoking, 45% in men and 10% in women by alcohol drinking, 40% in men and 29% in women by a diet poor in fresh fruit and vegetables. Altogether, these 3 factors – tobacco, alcohol and poor diet – accounted for 90% of cases in Italian men and 58% in women (83% in both sexes combined).
A case-control study of lung cancer incidence among women in Shenyang, China explored the relationship between diet and lung cancer risk, with emphasis upon the potential effects of specific dietary nutrients in being able to modify lung cancer risk (Zhou et al. 1999) Dietary information regarding 290 cases and population-matched controls was obtained using personal interviews. There was a significant difference between cases and controls with respect to intake of beta-carotene, vitamin C, and fibre, all of which reduced the risk for lung cancer in a dose-dependent manner, with calculated odds ratio (OR) of 0.84, 0.75, and 0.46, respectively. The apparent effects of these nutrients persisted after adjusting for cigarette smoking. The authors’ conclusions were that beta-carotene, vitamin C, and fibre may function as protective factors to reduce the risk of lung cancer in women in China.
Breast cancer is a serious health problem, accounting for almost one-third of cancer-related deaths in women in America (Kimmick et al. (1997). As the prevention of breast cancer using dietary modification is an active area of clinical and epidemiological research, it has been proposed that vitamin E supplementation may reduce a woman’s risk of developing breast cancer. The authors review (60 references) the available evidence regarding vitamin E and breast cancer.
Vitamin E has decreased incidence of carcinogen-induced breast tumours in animal studies. However, there have been conflicting results in human epidemiological research. Further study is warranted, particularly regarding its interactions with other antioxidants and to the duration and timing – pre- vs postmenopausal – of vitamin E use to determine its use in the treatment and prevention of breast cancer.
Nutritional evidence at the cell and molecular level
The potential antiproliferative effects of tocotrienols, the vitamin E component in palm oil, upon human breast cancer cell growth have been studied by Nesaretnam et al. (1998). Both oestrogen-responsive (ER+) MCF7 and oestrogen- unresponsive (ER-) MDA-MB-231 human breast cancer cells were used in this study. The effects of the tocotrienol-rich fraction (TRF) of palm oil were compared with those of alpha-tocopherol (alphaT).
TRF inhibited growth of MCF7 cells (ER+) both in the presence and absence of oestradiol; the dose-response was nonlinear, and complete suppression of growth was achieved at 8 µg/ml. MDA-MB-231 (ER-) cells were also inhibited by TRF; there was a linear dose-response and complete growth suppression was achieved with 20 µg/ml. Fractionation of the TRF into individual tocotrienols revealed that all the fractions inhibited the growth of both ER+ and ER- cells, and of ER+ cells both in the presence and absence of oestradiol. The most highly inhibitory were the gamma- and delta-fractions; complete inhibition of MCF7 cell growth was achieved at 6 µg/ml of gamma-tocotrienol/delta-tocotrienol (gammaT3/deltaT3) in the absence of oestradiol and 10 µg/ml of deltaT3 in the presence of oestradiol. Complete suppression of growth of MDA-MB-231 (ER-) cells was not achieved even at concentrations of 10 µg/ml deltaT3. In contrast to the inhibitory effects of tocotrienols, alphaT had no inhibitory effect upon MCF7 nor on MDA-MB-231 cell growth either in the presence or absence of oestradiol.
These data confirm results from other studies using other sublines of human breast cancer cells and demonstrate that tocotrienols exert direct inhibitory effects upon breast cancer cell growth. Studies of the effects of the tocotrienol-rich fraction (TRF) upon oestrogen-regulated pS2 gene expression in MCF7 showed that tocotrienols do not act via an oestrogen receptor-mediated pathway and must therefore act differently from oestrogen antagonists. Also, tocotrienols did not increase levels of growth-inhibitory insulin-like growth factor binding proteins (IGFBP) in MCF7 cells, implying a different mechanism from the one proposed for retinoic acid inhibition of oestrogen-responsive breast cancer cell growth.
The inhibition of breast cancer cell growth by tocotrienols may have important clinical implications not only because tocotrienols inhibit the growth of both ER+ and ER- cell types, but also because ER+ cells could be growth-inhibited in the presence as well as in the absence of oestradiol. Future clinical applications of TRF may arise from potential growth suppression of ER+ breast cancer cells which are resistant to growth inhibition by antioestrogens and retinoic acid.
The antitumour effect of the herbal medicine sho-saiko-to and its mechanism of action upon a murine malignant melanoma cell line (Mel-ret) was studied by Liu et al. (1998). Sho-saiko-to induced apoptotic cell death of Mel-ret cells with a definite increase of cell surface Fas antigen and Fas ligand (FasL). [Fas is a protein recognition / signalling pathway.] Sho-saiko-to arrested Mel-ret cells in G1 phase (a phase during cell division) by decreasing the expression of cyclin-dependent kinase (cdk) 4 and its homologue cdk6. Kinase activities of cdk4 and cdk6 were shown to be downregulated by sho-saiko-to. Ingredient analysis revealed that baicalin is likely to be the main active constituent in the upregulation of Fas antigen and Fas ligand, while glycyrrhizin is the main constituent in the inhibition of cyclin-dependent kinases.
Zheng et al. (1997) recognized that various naturally occurring substances from vegetables and herbs exert chemopreventive properties against cancer. The authors reviewed two such compounds, isolated from garlic and from a traditional Chinese medicinal herb, elemene, isolated from the herb Rhizoma zedoariae.
Elemene was shown to exhibit antitumour activity in human and murine tumour cells both in vitro and in vivo and has shown substantial clinical activity against various tumours. Analysis by MTT assay of the effect of elemene upon the growth of leukaemia cells showed that the IC50 for promyelocytic leukaemia HL-60 cells and erythroleukaemia K562 cells were 27.5 µg/ml and 81 µg/ml respectively, and the IC50 for peripheral blood leukocytes PBL) was 254.3 µg/ml. Inhibition of elemene upon the proliferation of HL-60 cells was associated with cell cycle arrest from S to G2M phase transition, and with the induction of apoptosis. The apoptosis of tumour cells was confirmed by DNA ladder formation using gel electrophoresis and ultrastructural alterations.
The results also demonstrated that the inhibitory effects of allicin, a natural organosulphide from garlic, upon the proliferation of tumours cells were associated with the cell cycle blockage of S/G2M boundary phase and the induction of apoptosis.
These results suggest that the induction of apoptosis may contribute to the mechanisms of antitumour activity of elemene and allicin, which deserve further investigation as potential chemoprevention agents in humans.
The mechanism by which vitamin A prevents or delays carcinogenesis is still unclear (Maziere et al. 1997). Vitamin A, in addition to antimutagenic and antiproliferative properties, also appears to be able to induce programmed cell death (apoptosis). The authors studied the role of vitamin A regarding in vitro apoptosis induction in a rat colon tumour cell line. Retinyl palmitate in varying concentrations was added to the culture media. Cell proliferation was measured via (3H)thymidine incorporation, cell differentiation via intestinal alkaline phosphatase expression and apoptosis induction by DNA fragmentation and morphological evolution of adherent and floating cells.
Vitamin A decreased (3H)thymidine incorporation following 1 day of treatment, induced alkaline phosphatase expression and increased cells undergoing apoptosis. This study confirms the role of vitamin A regarding proliferation and demonstrates the capacity of vitamin A to induce apoptosis. These results may be useful to prevent development of colon cancer by supplementation of the diet with vitamin A.
Roles of individual nutrients and foods
Proposed mechanisms of vitamin C (ascorbic acid, ascorbate) for cancer treatment and prevention were reviewed by Head (1998). They include immune system enhancement, stimulation of collagen formation for ‘walling off’ tumours, inhibition of hyaluronidase to keep intact the ground substance around the tumour and prevent metastasis, prevention of oncogenic viruses, correction of ascorbate deficiency frequently observed in cancer patients, speeding up of wound healing following cancer surgery, enhancement of various chemotherapy drugs, reduction of toxicity of chemotherapeutic agents such as Adriamycin, prevention of damage from free radicals, and neutralization of carcinogenic substances.
Published studies from Scotland and Japan have reported the potential benefit of high dosages of vitamin C in the treatment of terminal cancer. Studies from the Mayo Clinic disputed those findings, resulting in acrimonious accusations of methodological flaws from both sides. Numerous epidemiological studies have demonstrated the importance of dietary and supplemental vitamin C in the prevention of numerous cancers, including bladder, breast, cervical, colorectal, oesophageal, lung, pancreatic, prostate, salivary gland, stomach, leukaemia and non-Hodgkin’s lymphoma.
Animal research studies
The effect of diet treatments with soy flour and rye bran upon prostate tumour development was investigated by Landstrom et al. (1998). 125 rats with transplanted R3327 PAP prostate tumours were divided into five groups. Tumour development was studied for 24 weeks during treatment with diets containing: 1) 33% soy flour (SD); 2) rye bran (RB); 3) heat-treated rye bran (HRB); 4) rye endosperm (RE); 5) control, fibre-free dietary (FF).
Compared with the control (FF), there were significantly fewer palpable tumours and lower tumour volume detected 14 and 16 weeks following transplantation in the SD (soy), RB (rye bran), and HRB (heat-treated rye bran) groups. Compared with the control, body weight was lower 16 weeks after transplantation in the RB and HRB groups. There was a significantly lower energy intake in the RB and HRB groups, compared with the controls during the 3-6 weeks following tumour transplantation, whereas energy intake was the same in all groups 13-16 weeks following transplantation. Even following adjustment of tumour volume for body weight, there were still significantly lower tumour volumes in the SD, RB, and HRB groups compared with the FF controls. There was a significant increase in daily urinary excretion of the isoflavonoids daidzein, O-desmethylangolensin, equol and Genistein in the SD group, and of the ligands enterolactone and enterodiol in the RB and HRB groups. There were no differences in testosterone levels between the groups.
These data show that soy flour inhibits implanted prostate cancer growth. Rye bran and heat-treated rye bran had a protective effect; however further studies are required to exclude the possibility that a low energy intake may have played a role in this regard. These results also suggest that phytoestrogens, isoflavonoids, and ligands may be responsible for the delayed prostate tumour growth.
Kishimoto et al. (1998) studied the effectiveness of vitamin E in the prevention of lung cancer in mice. NNK (4-(methylnitrosamino)-1-(3-pyridyl)-1-butanone was the chemical agent used to induce lung tumours. High doses of vitamin E suppressed NNK-induced increased activity of ornithine decarboxylase, a key enzyme of polyamine biosynthesis, in the lungs of mice 4 weeks following injection. Vitamin E, in contrast, increased the NNK-induced decrease of spermidine/spermine N1-acetyltransferase activity, a key enzyme of polyamine biodegradation. Vitamin E treatment suppressed NNK-increased levels of proliferating nuclear cell antigen, a marker of cell proliferation, and high doses of vitamin E suppressed NNK-induced lung tumourigenesis, i.e. inhibiting the development of lung tumours. The mechanism of inhibition is in part due to the regulation of polyamine metabolism.
Beta-carotene (BC) has been found to possess potent antitumour activity in liver carcinogenesis chemically induced by diethylnitrosamine (DEN) in rats Sarkar et al. (1997). The authors studied the basic cytogenetic and molecular mechanisms of the antitumour effects of beta-carotene. They monitored the effect of beta-carotene upon rat liver chromosomal aberrations (CAs) and DNA chain breaks in the early precancerous stage of liver cancer in rats. Even one DNA strand break per chromosome can be detected. A BC supplement, 120 mg/kg was fed to rats 15 days prior to challenge with a carcinogenic chemical.
Beta-carotene provided a unique protection against chromosomal strand breaks 96 hours following injection of DEN. Long-term treatment also afforded a protective effect on induction of CAs 15, 30 and 45 days following DEN treatment. Beta-carotene treatment for 15 days prior to DEN injection offered significant protection in the generation of single-strand breaks compared with DEN control. Beta-carotene ranks as a potential chemopreventive agent regarding rat liver carcinogenesis.
Human research studies
A cross-sectional study of postoperative non-small cell lung cancer (NSCLC) patients looked at the possible effects of vitamin intake and folate status upon disease-free survival Jatoi et al. (1998). Supplemental vitamin usage, dietary vitamin intake, red blood cell (RBC) folate, and serum folate concentrations were assessed in 36 patients with a history of NSCLC. Exclusion criteria included factors altering folate status or associated with altered nutritional habits: 1) evidence of cancer on history, physical, or chest radiograph; 2) tobacco, alcohol ingestion (>2 drinks/day) or cancer treatment within 3 months; 3) the use of folate antagonists; and 4) age <60 years.
The median disease-free censored survival was 24 months (range 4-41 months). 19 of 36 patients (53%) reported vitamin supplementation. Compared with non vitamin supplement users, vitamin users had a longer median censored survival (41 months versus 11 months, P = 0.002). Following adjustment for stage of cancer, the association between RBC folate and censored survival (r = 0.35) and serum folate and censored survival (r = 0.32) approached statistical significance. Thus those patients with NSCLC who took vitamin supplements were more likely to be long-term survivors. A similar trend toward long-term survival was seen in patients with higher circulating folate concentrations.
Sixty cancer patients with secondary lymphoedema, with particular reference to the development of the incidence of erysipelas (acute, streptococcal inflammation of the skin and subcutaneous tissues, infection accompanied by fever and constitutional disturbances) took part in a randomized, double-blind study to determine the efficacy of sodium selenite in combination with physical therapy to relieve congestion (Kasseroller 1998). All the patients in this study had erysipelas infection of the skin. Selenium was administered in pharmacological doses. Physical therapy was for 3 weeks and patients were observed for a further 3 months.
The incidence of erysipelas among the patients was 11%. During the 3-week period of intensive treatment, there was not a single case of erysipelas in the treatment, compared with a single case in the placebo group. During the follow-up period of 3 months, there was not a single case of erysipelas in the treatment group, compared with 50% of the patients in the placebo group. Despite the higher doses, the selenium level did not rise above normal values. Patients under long-term antibiotic therapy suffered no relapse when the antibiotic therapy was stopped and selenium was administered instead. Additionally, the administration of a single high-dose of sodium selenite could immediately bring the inflammation under control.
In another trial, 974 men with a history of either basal cell or squamous cell cancer were randomized to receive a daily supplement of 200 µg of selenium or a placebo to test whether supplemental dietary selenium is associated with changed incidence of prostate cancer. The men were treated for a mean of 4.5 years and followed for a mean of 6.5 years (Clark et al. 1998).
Selenium treatment was associated with a significant (63%) reduction in the secondary endpoint of prostate cancer incidence during 1983-93. There were 13 prostate cancer cases in the selenium-treated compared with 35 in the placebo group (relative risk RR = 0.37). If the analysis is restricted to the 843 patients with initially normal levels of prostate-specific antigen (PSA), there were only 4 cases diagnosed in the selenium-treated group compared with 16 in the placebo group following a 2-year treatment lag (RR = 0.26). Other significant health benefits were observed for the secondary endpoints of total cancer mortality and incidence of total, lung and colorectal cancer. There were no significant changes in incidence for primary endpoints of basal and squamous cell skin cancer. In the light of these results, the ‘blinded’ phase of this trial was stopped early. In conclusion, selenium treatment was associated with substantial reductions in the incidence of prostate cancer and total cancer incidence and mortality. Selenium did not show a protective effect against squamous and basal skin cancers.
Peng et al. (1998) analysed the plasma concentrations of 10 micronutrients in cervical tissue from cancerous, precancerous, and noncancerous women. Paired blood and cervical tissue samples were taken from 87 patients, aged from 21-86 years who had a hysterectomy or biopsy due to cervical cancer, precancer (cervical intraepithelial neoplasia I, II and III), or noncancerous diseases. The samples were analysed for 10 micronutrients (lutein, zeaxanthin, beta-cryptoxanthin, lycopene, alpha-carotene, beta-carotene, cis-beta-carotene, alpha-tocopherol, gamma-tocopherol and retinol).
In the three patient groups, the mean plasma concentrations of all micronutrients except gamma-tocopherol were lowest in the cancer patients; however, the mean tissue concentrations of the two tocopherols and certain carotenoids were highest in the cancerous tissue. Among the 10 micronutrients, only the concentrations of beta-carotene and cis-beta-carotene were lower in both the plasma and tissue of cancer and precancer patients than in those of noncancer controls. These data suggest that not all the micronutrient concentrations in plasma reflect the micronutrient concentrations in cervical tissue. In some cases, it may be necessary to measure the tissue micronutrient concentrations in order to define the role of the micronutrients in cervical cancer. An adequate plasma and tissue concentration of beta-carotene should be maintained for the prevention of cervical cancer and precancer.
To investigate whether dietary supplements of selenium (Se) reduce the risk of cancer 1312 patients with histories of basal/ squamous cell carcinomas, recruited from 1983-1990 were randomly assigned in double-blind fashion to daily oral supplements of either Se-enriched yeast (200 µg/Se/day) or a low-Se yeast placebo (Combs et al. 1997). Patients were followed with regular dermatological examinations through to 1993, representing 8269 person-years of observation. Skin cancer diagnoses were confirmed histologically, plasma selenium concentrations were determined at 6-12 month intervals, and deaths and patient illnesses were recorded, confirmed, and documented in consultation with medical care providers. Although selenium did not significantly affect the primary endpoints, incidence of recurrent basal/squamous cell skin cancer, selenium treatment was associated with reduction in a number of secondary endpoints: total mortality from all cancers, combined incidence of all cancers, combined lung cancer, colorectal cancer and prostate cancer.
These results strongly demonstrated the benefits of Se-supplementation, supporting the hypothesis that supplemental Se can reduce cancer risk. Despite the lack of protective effects against non-melanoma skin cancer, the reductions in risk of other frequent cancers demand further evaluation in controlled clinical intervention trials.
There is no doubt from the few examples cited above that much research has already been conducted and is ongoing regarding the application of nutrition in both the prevention and treatment of cancer. However, more concerning is the virtual non-translation of these findings into either medical or people’s lifestyle practices. Considering the ageing of the developed world’s population and the rising incidence of cancer, associated with lifestyle, environmental and dietary factors, and the human and monetary costs of cancer, social, environmental, and lifestyle issues need to be addressed. It would help if the medical profession appeared to be cognisant of the huge body of evidence already amassed, rather than always attempting to deride and denigrate the use of nutritional approaches to cancer treatment.
Today there are also a variety of non-mainstream nutritional therapeutic practices – various dietary regimes such as Gerson, macrobiotics, Vries, wheat grass, fasting, colon cleansing, herbal regimes – espoused by a variety of practitioners which may be scorned by the general medical community, but which, if subjected to serious and concerted research, may reveal significant therapeutic efficacy. Today’s marginal practice may become tomorrow’s mainstream clinical protocol. There is an urgent requirement for research regarding the efficacy of these nutritional and dietary cancer regimes in treatment of cancer patients, and the decriminalization of nutrition as a cancer treatment methodology.
A few selected areas of education, policy and research requiring urgent attention include:
* The addition of nutrition into the medical school curriculum;
* The improved communication of published research to physicians and the systemic and comprehensive integration of published findings into clinical practice;
* The requirement of open and vigorous debate about fundamental precepts such as RDAs (recommended daily allowances), balanced diet, and the use of supplements;
* The necessity for serious research about the many and varied dietary regimes currently being advocated and used by many tens of thousands of people, who claim efficacy, particularly for cancer – vegetarian, frugivore, raw food, macrobiotic, Gerson diet, fasting;
* The identification and research of components within vegetables and other foods which appear to protect against cancer;
* Research of anti-oestrogen foods such as soybeans and their preventive effects in cancer.
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This article is extracted with permission from Integrated Cancer Care, ed. Jennifer Barraclough, Oxford University Press, 2001.© Sandra Goodman 2001.