| 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).
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