From: Technotranscendence (neptune@mars.superlink.net)
Date: Sat Mar 24 2001 - 09:40:46 MST
LIFE EXTENSION UPDATE, MARCH 23 2001
IN THIS ISSUE, MARCH 23 2001:
LIFE EXTENSION UPDATE EXCLUSIVE: Indole-3-carbinol kills ovarian cancer
cells and boosts chemotherapy;
WHAT'S HOT: Another cancer associated with hormone replacement therapy;
PROTOCOL: Cancer Surgery;
FEATURED PRODUCTS OF THE WEEK: Indole-3-carbinol, Modified Citrus Pectin;
LIFE EXTENSION MAGAZINE: Vegetables without vitamins;
JOIN THE LIFE EXTENSION FOUNDATION
LIFE EXTENSION UPDATE EXCLUSVIE
Life Extension Update Exclusive brings you news each week that you will
only receive in the ezine.
Indole-3-carbinol kills ovarian cancer cells and boosts chemotherapy
In a study presented at the thirty-second annual meeting of the Society of
Gynecologic Oncologists held this month, researchers from North Shore/Long
Island Jewish Research Institute and North Shore/Long Island University
Hospital presented the results of a National Cancer Institute funded study
that showed indole-3-carbinol and its product diindolylmethane (DIM) both
had a toxic effect on ovarian cancer cells in vitro. Indole-3-carbinol is
a phytonutrient found in cruciferous vegetables such as broccoli and
cabbage that has been demonstrated to have cancer preventive properties as
well as the ability to slow the progression of some cancers. The authors
note that it is currently being used to prevent human papilloma virus
related cancers.
Two ovarian cancer cell lines were treated with indole-3-carbinol or DIM
in various concentrations for two to four days. Cell viability was
measured by mitochondrial function. Both indole-3-carbinol and DIM showed
toxicity to both lines after a two day period. The two substances were
then combined with the cancer chemotherapy drug cis-platinum to test their
effects. Both compounds enhanced the toxicity of the drug toward the
cancer cell line known as OVCAR-3, known to be resistant to cis-platinum.
The combination of cis-platinum and another chemotherapeutic drug,
paclitaxel, was able to kill 70% of the ovarian cancer cells in this line,
but when diindoylmethane was added it resulted in complete destruction of
the cells. Diindoylmethane alone in one concentration was able to kill all
of the cells in the other ovarian cancer cell line in a matter of four
days.
The researchers believe that both indole-3-carbinol and diindoylmethane
will prove useful as adjunctive agents in ovarian cancer management and
note that further studies are in progress.
WHAT'S HOT
Another cancer associated with hormone replacement therapy
The use of hormone replacement therapy (HRT) by women during and following
menopause has recently been found to be linked with an elevated risk of
breast and endometrial cancer, as well as failing to protect against
cardiovascular disease. A large study published in the March 21 2001 issue
of the Journal of the American Medical Association shows that hormone
replacement appears to increase the risk of ovarian cancer as well.
Ovarian cancer is usually detected in its late stages making it difficult
to treat.
The study utilized data from the American Cancer Society's Cancer
Prevention Study II, which followed up participants for mortality from
1982 to 1996. Of the 676,526 people enrolled in this study who completed
questionnaires in 1982, there were 211,581 postmenopausal cancer-free
women who did not report a hysterectomy. During the fourteen year
follow-up period, 944 members of this group succumbed to death from
ovarian cancer.
Twenty-two percent of the women reported noncontraceptive hormone
replacement use on their questionnaires. The highest risk of ovarian
cancer was found in women who had used hormone replacement therapy for ten
or more years. This risk was present up to twenty-nine years after hormone
replacement was discontinued. Those who were using hormone replacement the
most recently experienced a higher risk than those who had previously used
it. Women who had used HRT for less than ten years had a small but
insignificant increased risk. The lowest risk of ovarian cancer was found
in women who had never been on HRT, in whom an annual age-adjusted death
rate from ovarian cancer was 26.4 per 100,000 women, compared to that of
64.4 for those who were on HRT at the beginning of the study and who had
used it for ten or more years.
The authors postulate two mechanisms of action for postmenopausal
estrogen: decreased gonadotropins caused by elevated serum estradiol and
estrone levels, or a direct effect of estrogen on ovarian cells. They
state that if their results are confirmed, clinicians will need to add
ovarian cancer to the list of longterm estrogen use risks.
http://www.lef.org/cgi-local/welcome.cgi/id=151063007/sgroup_id=699/welcome.
html
PROTOCOL
Cancer Surgery
Surgery poses many risks to a cancer patient. The known side effects
associated with the surgical removal of tumors include anesthesia
complications, infections, and immune suppression. A newly discovered
surgery side effect of concern to cancer patients is that the removal of
the primary tumor may directly stimulate the propagation of metastatic
lesions. The theory is that an intact primary tumor regulates the growth
of metastatic lesions by naturally secreting antiangiogenesis agents such
as endostatin and angiostatin. Metastatic tumors require the formation of
new blood vessels (called angiogenesis) in order to grow. Once the primary
tumor has been surgically removed, the amount of endostatin and
angiostatin to control new blood vessel growth is drastically reduced, and
metastasized lesions begin proliferating out of control. If the immune
depression that surgery induces is factored in, the failure of surgery to
meaningfully prolong the life of cancer patients becomes quite
understandable. Surgery takes away growth control factors (endostatin and
angiostatin) while simultaneously weakening the immune surveillance that
might be keeping metastatic lesions under some degree of control.
Almost every tissue in the body derives blood from the thinner-than-a-hair
capillaries that lace our tissues. Through capillaries, nutrients, oxygen
and various signaling molecules diffuse into cells. These mechanisms
maintain health, fight disease, and allow the body to flourish and grow.
Scientists have found that tumors start out without circulation. In the
early stages of tumor development, they are limited to a trickle of
nutrients that can diffuse from the nearest capillaries. Then, somehow,
tumors begin to stimulate healthy tissue to make thousands of new blood
vessels to supply the cancerous growth-a process called angiogenesis.
Without this ability to nourish itself and grow, a tumor cannot enlarge.
If the blood supply can be reduced or cut off, the tumor will shrink or
die.
http://www.lef.org/cgi-local/welcome.cgi/id=151063008/sgroup_id=699/welcome.
html
FEATURED PRODUCTS OF THE WEEK
Indole-3-carbinol
Strong evidence suggests that the risk of many cancers can be reduced by
eating lots of broccoli, cabbage, cauliflower and other cruciferous
vegetables. The problem is that the amount of cancer fighting compounds
varies in each crop harvested, and most people just don't eat enough
cancer-preventing vegetables on a consistent basis. Food scientists have
isolated indole-3-carbinol and are making it available to the supplement
market for the first time at an affordable price. The Life Extension
Foundation has been publishing information about indole-3-carbinol since
1983, and a summary of recent studies shows that this vegetable extract:
Increased the conversion of estradiol to the safer estriol by 50% in
twelve healthy people in just one week.
Prevented the formation of the carcinogenic estrogen metabolie
16-alpha-hydroxy estrone in two months in 17 men and women.
Stops human cancer cells from growing (54-61%) and provokes the cells to
self-destruct (apoptosis).
Inhibits MCF7 human breast cancer cells from growing by as much as 90% in
culture.
Inhibits an estrogen metabolite (16-alpha-hydroxyestrone) that prompts
breast cancer cells to grow.
Competes with dioxin for the Ah receptor to help keep dioxin out of cells.
Prevented chemically-induced breast cancer in rodents by 70-96% Prevented
other types of cancer, including aflatoxin-induced liver cancer, leukemia
and colon cancer.
Inhibits free radicals, particularly those that cause the oxidation of
fat.
Inhibits the growth of estrogen receptor-positive breast cancer cells by
90%, compared to tamoxifen's 60%, by stopping the cell cycle.
Stopped the synthesis of DNA for new cells by about 50% in estrogen
receptor-negative cells whereas tamoxifen had no significant effect.
Restores p21 and other proteins that act as check points during the
synthesis of a new cancer cell. Tamoxifen has no effect on p21.
Virtually eliminated DNA damage and cancer when animals were fed it before
exposure to cancer-causing chemicals.
Reduced DNA damage in breast cells by 91%. Similar results happen in the
liver.
Reduces levels of a major carcinogen in female smokers.
http://www.lef.org/cgi-local/welcome.cgi/id=151063009/sgroup_id=699/welcome.
html
Modified Citrus Pectin
Cancer cell metastasis is the mechanism of disease progression that leads
to death for most cancer patients. A special pH-altered form of citrus
pectin has been shown to interfere with cancer cell metastasis by
inhibiting the ability of cancer cells to adhere to other cells in the
body. It inhibits metastasis by interfering with cellular interactions
that are required for the transport and proliferation of tumor cells to
secondary sites in the body.
Additional research on Modified Citrus Pectin shows that it enhances the
activity of natural killer immune cells, which are required to destroy
migrating cancer cells in the bloodstream.
http://www.lef.org/cgi-local/welcome.cgi/id=151063010/sgroup_id=699/welcome.
html
LIFE EXTENSION MAGAZINE, MARCH 2001
Vegetables without vitamins
That's what happened to nutritionist, Alex Jack, when he went to check out
the latest US Department of Agriculture food tables. The stunning
revelation came after Jack compared recently published nutrient values
with an old USDA handbook he had lying around. Some of the differences in
vitamin and mineral content were enormous-a 50% drop in the amount of
calcium in broccoli, for example. Watercress down 88% in iron content;
cauliflower down 40% in vitamin C content-all since 1975.
Jack took his findings to the USDA, hoping for a reasonable explanation.
That was two years ago. He's still waiting. So is Organic Gardening
magazine, which published an open letter, seeking an explanation from Dan
Glickman, Secretary of Agriculture. Glickman didn't respond, but USDA
employee, Phyllis E. Johnson did. Johnson (who is head of the Beltsville
area office), suggested to Organic Gardening that the nutrient drain
should be put in context. According to her, the 78% decrease in calcium
content of corn is not significant because no one eats corn for calcium.
She further explains that the problem may not even exist at all; that the
apparent nutrient dips could be due to the testing procedures. For
example, "changes in the public's perception of what the edible portion is
may determine what parts have been analyzed over time." In other words,
back when the old food tables were made up, people may have been eating
the cobb too, so they got more nutrients.
http://www.lef.org/cgi-local/welcome.cgi/id=151063011/sgroup_id=699/welcome.
html
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Foundation membership entitles you to obtain supplements from the Life
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http://www.lef.org/cgi-local/welcome.cgi/id=151063012/sgroup_id=699/welcome.
html
Visit our website at www.lef.org
If you have any questions or comments concerning this issue or past issues
of Life Extension Update, or on any other life extension topic, please
send them to me at ddye@lifeextension.com
For longer life,
Dayna Dye
Editor, Life Extension Update
ddye@lifeextension.com
Life Extension Foundation
www.lef.org
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