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| Life Extension Update Exclusive
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. |
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| Protocol
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 [PSA]). 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).
http://www.lef.org/protocols/prtcl-027.shtml
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For longer life,
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Editor, Life Extension Update
ddye@lifeextension.com
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