SeMC - Related Research

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%

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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