The most potent,
least toxic selenium supplement ever!
Selenium is now well established
as a potent cancer-fighting trace mineral. Areas of the world
with more selenium-rich soil have lower cancer rates, and
a randomized, double-blind, placebo-controlled trial in the
1990s showed that men taking a daily 200 microgram selenium
supplement experienced a 37% lower risk of developing new
cancer, and a whopping 50% lower risk of cancer death.
But not all forms of selenium
are equal in their cancer-fighting properties. To everyone’s
surprise, the last decade of scientific research has found
that selenium’s anticancer effect is not due to its
use as part of antioxidant or detoxifying compounds in the
body. It’s also not linked to absolute tissue levels
of selenium achieved by a given form of selenium, or to its
ability to boost the immune system. Instead, the cancer-fighting
potency of any form of selenium is linked to its ability
to form methylselenol, a critical selenium metabolite in
the body.
As a result of this research,
science has identified Se-methylselenocysteine, or SeMC,
as a form of selenium which is directly and easily converted
into this key cancer-fighting metabolite – unlike conventional
inorganic (selenite or selenate) or organic (selenomethionine,
or selenized yeast) selenium supplements. As a result, SeMC
is simultaneously more potent in its cancer-battling prowess,
and less toxic per unit of cancer-fighting punch, than any
other selenium supplement available.
• SeMC is twice as effective
as selenomethionine at reducing breast tumor formation after
exposure to the chemical carcinogens dimethylbenz[a]anthracene
(DMBA) and methylnitrosourea (MNU), and half again as effective
as inorganic forms.
• At the same time, SeMC is much safer than inorganic selenium, and of comparable
safety to the much less-effective selenomethionine.
SeMC Against Experimental
Breast Cancer
To
Cut Tumors by 50%
Form Of Selenium |
Dose (ppm) |
Toxic Dose (ppm) |
| SeMC |
2 |
5 |
Selenite |
3 |
4 |
| Selenomethionine |
4-5 |
5-6 |
SeMC is the main form of selenium
that accumulates in known cancer-fighting foods like broccoli,
ramps, garlic, and (to a lesser extent) onions when grown
in selenium-rich soil. Studies high-SeMC-cultivars of these
vegetables suggest that SeMC is a key element in the cancer-fighting
efficacy of these protective vegetables.
• High-SeMC broccoli gives
animals more protection against early-stage colon cancer
than does an equal amount of conventional selenium, an equal
amount of regular broccoli, or even a combination of both.
• Similar results are seen in battling abnormal cells that lead to breast
or colon cancer using high-SeMC garlic vs. the same amount of selenium from high-selenomethionine
yeast or Brazil nuts.
• SeMC is proven effective in an animal model of familial adenomatous polyposis
(FAP), a human genetic vulnerability to colon cancer. No other natural selenium
compound has been shown to do this.
Unique Mechanisms of Action: SeMC
fights cancer in ways fundamentally different from other
selenium forms.
• Apoptosis vs Necrosis:
Inorganic selenium kills cancer cells through nonselective
damage to the DNA and cell membranes of both healthy cells
and cancer cells, leading to toxic cell death (necrosis).
SeMC selectively activates cancer cells’ “suicide
program” (apoptosis) without damage to healthy cells.
• Gene expression: SeMC regulates cellular growth programs, inhibiting cancer
cells earlier in the cell cycle than does inorganic selenium.
• Angiogenesis: SeMC may also act by cutting off the growing tumor’s
blood supply more effectively than the common selenium supplements, without interfering
with the growth of blood vessels in normal, healthy tissue.
By any measure, SeMC has proved
itself to be the best selenium you can take. The National
Cancer Institute apparently agrees: it is in the process
of filing “Investigational New Drug” documents
to use SeMC instead of other selenium supplements in future
human trials.
References
i. Whanger PD. “Selenocompounds
in plants and animals and their biological significance.” J
Am Coll Nutr. 2002 Jun; 21(3): 223-32.
ii. Medina D, Thompson H, Ganther
H, Ip C. “Se-methylselenocysteine: a new compound for
chemoprevention of breast cancer.” Nutr Cancer. 2001;
40(1):12-7.
iii. Ip C. “Lessons from
basic research in selenium and cancer prevention.” J
Nutr. 1998 Nov; 128(11): 1845-54.
iv. Finley JW, Davis CD. “Selenium
(Se) from high-selenium broccoli is utilized differently
than selenite, selenate and selenomethionine, but is more
effective in inhibiting colon carcinogenesis.” Biofactors.
2001; 14(1-4): 191-6.
v. Ip C, Birringer M, Block E,
Kotrebai M, Tyson JF, Uden PC, Lisk DJ. “Chemical speciation
influences comparative activity of selenium-enriched garlic
and yeast in mammary cancer prevention.” J Agric Food
Chem 2000 Jun; 48(6): 2062-70.
vi. Ip C, Hayes C, Budnick RM,
Ganther HE. “Chemical form of selenium, critical metabolites,
and cancer prevention.” Cancer Res 1991 Jan 15; 51(2):
595-600.
vii. Jiang C, Wang Z, Ganther
H, Lu J. “Caspases as key executors of methylselenium-induced
apoptosis (anoikis) of DU-145 prostate cancer cells.” Cancer
Res. 2001 Apr 1; 61(7): 3062-70.
viii. Finley JW, Ip C, Lisk DJ,
Davis CD, Hintze KJ, Whanger PD. “Cancer-protective
properties of high-selenium broccoli.” J Agric Food
Chem. 2001 May; 49(5): 2679-83.
ix. Ip C, Lisk DJ. “Characterization
of tissue selenium profiles and anticarcinogenic responses
in rats fed natural sources of selenium-rich products.” Carcinogenesis.
1994 Apr; 15(4): 573-6.
x. Yeo JK, Cha SD, Cho CH, Kim
SP, Cho JW, Baek WK, Suh MH, Kwon TK, Park JW, Suh SI. “Se-methylselenocysteine
induces apoptosis through caspase activation and Bax cleavage
mediated by calpain in SKOV-3 ovarian cancer cells.” Cancer
Lett. 2002 Aug 8; 182(1): 83-92.
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