25 februari 2012: ik ben kanker-actueel aan het herzien en laat dit artikel staan omdat het nog steeds relevante informatie geeft naar mijn mening

8 september 2004: Bron: http://www.lef.org Life Extension

Groenten en aanvullend betacaroteen, een vitamine-B complex en vitamine E zouden het risico op het krijgen van eierstokkanker aanzienlijk verminderen, aldus een epidemologische studie onder 2500 vrouwen in Ottowa Canada. Zo meldt de nieuwsbrief van Life Extension, een organisatie en tijdschrift dat vooral aandacht geeft aan wetenschappelijk onderzoek naar natuurlijke middelen en voedingstoffen. Er lijkt volgens de onderzoekers sprake van ca. 25% minder kans op het krijgen van eierstokkanker wanneer een bepaalde hoeveelheid van deze stoffen wordt ingenomen. Vooral betacaroteen en vitamine B-complex geven een aanzienlijk effect, maar ook vitamine E. Opvallend ook dat het eten van eieren en cholesterol verhogend voedsel het risico op het krijgen van eierstokanker juist verhoogd.
We hebben nu geen tijd dit allemaal te vertalen, maar lees onderstaande Engelstalige publicatie, zoals deze ook gepubliceerd is in het Septembernummer 2004 van the journal Cancer Epidemiology, Biomarkers & Prevention .Het abstract daarvan staat onder artikel van Life Extension.

Vegetables, supplements lower ovarian cancer risk

A case-control study reported in the September 2004 issue of the journal Cancer Epidemiology, Biomarkers & Prevention has found an inverse association between the risk of developing ovarian cancer and the intake of vegetables and supplements of beta-carotene, B complex and vitamin E. Researchers from Ottawa, Ontario administered health history and dietary questionnaires to 442 women diagnosed with ovarian cancer and 2,135 age-matched women who were cancer free. Intake levels of foods and nutritional supplements for the two years preceding the study was analyzed by the researchers, and the groups were compared. In this study, women with ovarian cancer were more likely to be postmenopausal, to be obese, to have consumed more calories, to have had fewer births and to have lower physical activity levels than those without the disease. When diet was examined, no associations were found between ovarian cancer and intake of fat, protein, carbohydrates, and many other dietary components. Cholesterol and egg intake was associated with an insignificant increase in ovarian cancer risk. Women whose total vegetable intake and cruciferous vegetable intake was in the top 25 percent of participants experienced a risk of ovarian cancer that was almost one-fourth lower than those whose consumption was in the lowest quarter. When supplements were examined, women who took beta-carotene for over ten years had a risk of ovarian cancer that was 69 percent lower than those who did not report using the supplement. Vitamin E supplementation for the same period of time halved ovarian cancer risk. B-complex vitamins were associated with a smaller decreased risk. The authors attribute the vitamins' cancer preventive ability to their antioxidant capacity which helps prevent DNA damage, and note that vitamin E and beta-carotene also improve immune function. They recommend further study of B-complex's apparently less significant protective effect to confirm the current study's findings.

Cancer adjuvant therapy

The inhibitory role of vitamin E in the growth of a number of human tumor cells, as well as its defensive functions in overcoming treatment-induced toxicity have been examined. The impact of vitamin E (perhaps acting through its antioxidant strengths) is significant, as evidenced by the following studies:
After examining 29,000 male smokers in Finland, researchers found that high blood levels of alpha-tocopherol reduced the incidence of lung cancer by approximately 19%. The relationship appears stronger among younger persons and among those with less cumulative smoke exposure. These findings suggest that high levels of alpha-tocopherol, if present during the early critical stages of tumorigenesis, may inhibit lung cancer development (Woodson et al. 1999).
A combination of vitamin E and pentoxifylline (PTX), a drug that inhibits abnormal platelet aggregation, allowing more blood to reach irradiated areas, resulted in a 50% regression of superficial radiation-induced fibrosis (the proliferation of fibrous connective tissue) in half of the patients studied (Gottlober et al. 1996; Delanian 1998). A suggested dosage is 800 mg a day of PTX and 1000 IU per day of vitamin E.
An antimelanoma effect obtained from vitamin E succinate in vivo has been reported (Malafa et al. 2002). Gamma-tocopherol inhibits COX-2 activity, demonstrating anti-inflammatory properties (Jiang et al. 2001; Life Extension Magazine 2002).
The use of vitamin E, in combination with vitamins A and C, led to a four-fold reduction in p53 mutations (Brotzman et al. 1999). This is an extremely important finding because p53 mutations indicate a more malignant, aggressive form of cancer.
Men with a high intake of vitamin E are 65% less likely to develop colorectal adenomas (precursors to colon cancer) compared to men with low vitamin E intake (Tseng et al. 1996).
Lower morbidity and mortality from prostate cancer in men taking 50 mg of synthetic alpha-tocopherol daily. Subsequent testing determined gamma-tocopherol to be superior, however, to alpha-tocopherol in terms of tumor cell inhibition (Moyad et al. 1999). Men in the highest fifth of the distribution for gamma-tocopherol had a five-fold reduction in the risk of developing prostate cancer compared to those in the lowest fifth. In addition, statistically significant protection from high levels of selenium and alpha-tocopherol occurred only when gamma-tocopherol concentrations were also high (Helzlsourer et al. 2000). Vitamin E's mode of efficacy in regard to prostate protection: Vitamin E interferes with two proteins (the receptor for testosterone and prostate-specific antigen ). The fewer androgen receptors there are on a prostate cancer cell, the less capable the remaining receptors are of turning on genes that stimulate prostate cancer growth and progression. PSA serves as a good marker molecule for androgen receptor activity (Mercola 2002b).

Tocotrienols, quite similar to a tocopherol (but for the addition of an unsaturated tail in its chemical structure), accumulate in adipose tissues, including mammary glands. If a cell becomes diseased, the tocotrienol is prepared for action, ready to inhibit growth and regulate aberrant cellular activity at onset. Curiously, the more cancerous the cell, the more susceptible it is to tocotrienols. Scientists apparently have been focusing upon the wrong form of vitamin E (the tocopherols), which show little protection against breast cancer. Tocotrienols appear to inhibit proliferation of human breast cancer cells by as much as 50% (Nesaretnam et al. 1998). Results suggest that tocotrienols are effective inhibitors of both estrogen receptor-negative and estrogen receptor-positive cells and that combination with tamoxifen should be considered as a possible improvement in breast cancer therapy. This strategy could significantly reduce the amount of tamoxifen required to affect the cancer (Guthrie et al. 1997).
Cortisol (associated with poorer survival) and IL-6 (a negative marker for various cancers) were significantly lower in laboratory animals that received alpha-tocopherol before a cortisol-IL-6 challenge (Webel et al. 1998). Hierbij het abstract van de studie, zoals gepubliceerd in Cancer Epidemiology Biomarkers & Prevention Vol. 13, 1521-1527, September 2004:

A Case-Control Study of Diet and the Risk of Ovarian Cancer
Sai Yi Pan1, Anne-Marie Ugnat1, Yang Mao1, Shi Wu Wen2,3, Kenneth C. Johnson1 and The Canadian Cancer Registries Epidemiology Research Group 1 Surveillance and Risk Assessment Division, Center for Chronic Disease Prevention and Control, Population and Public Health Branch, Health Canada, Ottawa, Ontario, Canada; 2 OMNI Research Group, Department of Obstetrics and Gynecology, Faculty of Medicine, University of Ottawa, Ottawa, Ontario, Canada; and 3 Clinical Epidemiology Program, Ottawa Health Research Institute, Ottawa, Ontario, Canada

Requests for reprints: Dr. Anne-Marie Ugnat, Surveillance and Risk Assessment Division, Center for Chronic Disease Prevention and Control, Population and Public Health Branch, Health Canada, 120 Colonnade Road, Locator 6702A, Ottawa, Ontario, Canada K1A 0K9. Phone: 613-941-8498; Fax: 613-941-2057. E-mail: Anne-Marie_Ugnat@hc-sc.gc.ca

Epidemiologic studies have suggested that some dietary factors may play a role in the etiology of ovarian cancer, but the findings have been inconsistent. We assessed the association of ovarian cancer with dietary factors in a population-based case-control study in Canada. Diet information was collected on 442 incident cases of ovarian cancer diagnosed in 1994 to 1997 and 2,135 population controls via a self-administered questionnaire. Compared with women in the lowest quartile of cholesterol intake, those in the second, third, and fourth quartiles had a multivariate adjusted odds ratio [OR; 95% confidence interval (95% CI)] of 1.12 (0.81–1.56), 1.20 (0.85–1.68), and 1.42 (1.03–1.97), respectively (P for trend = 0.031). Higher egg consumption was also associated with a nonsignificant increase in ovarian cancer risk. The ORs (95% CIs) for ovarian cancer were 0.77 (0.60–1.04) and 0.76 (0.56–0.99) among women in the highest quartile of total vegetable and cruciferous vegetable intake as compared with women in the lowest quartile. Women who took supplements of vitamin E, ß-carotene, and B-complex vitamins for 10 years had ORs (95% CIs) of 0.49 (0.30–0.81), 0.31 (0.11–0.91), and 0.61 (0.36–1.05), respectively. However, we did not observe an association of ovarian cancer risk with dietary fat intake, including saturated, monounsaturated, and polyunsaturated fatty acids, protein, carbohydrate, dietary fiber, fruit, dairy products, meat products, fish, chicken, grain products, nut products, baked desserts, margarine, butter, mayonnaise, and supplement of multiple vitamins, vitamin A, vitamin C, calcium, iron, zinc, and selenium. Our findings suggested that ovarian cancer risk was positively associated with higher consumption of dietary cholesterol and eggs and inversely associated with higher intake of total vegetables and cruciferous vegetables and supplementation of vitamin E, ß-carotene, and B-complex vitamins.

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