beyond selenate . . . beyond selenomethionine . . . beyond whole selenized yeast . . .

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The Secret of Cancer-Fighting Foods

It’s long been known that people who live in areas with higher concentrations of selenium in their soil and crops are much less likely to die of cancer.1,3 And it’s well-established that a diet rich in fruits and vegetables is one of your best defenses against this killer – and especially certain specific fruits and veggies.49 The plant foods that have most consistently been found to lower your risk of cancer are cruciferous vegetables (such as broccoli and cabbage) and Allium vegetables (like onions and garlic), along with tomatoes.49 The usual explanation for these foods’ unique cancer-fighting properties is that aside from their vitamin content, these vegetables are vibrant sources of cancer-fighting phytonutrients.49 Thus, broccoli is a rich source of D-glucarate50 and sulforaphane51 (which support the detoxification of many cancer-causing compounds) as well as indole-3-carbinol52 (I3C, which supports the safer metabolism of potentially cancer-promoting estrogens), while garlic and onions are packed with diallyl disulfide, which favorably modulates your body’s handling of carcinogens.53

Once the remarkable cancer-fighting effects of SeMC came to light, however, scientists began to wonder if there might be a connection between the cancer-fighting powers of these vegetables and selenium – not just the amount of the mineral, but the kind. If the amount of selenium in a food was a reliable estimate of its anticancer effect, then wheat, barley, and corn would be more strongly associated with cancer protection than Brussels sprouts or chives, because these grains actually accumulate more selenium than cruciferous or Allium vegetables when grown in high-selenium soil.54 Yet the reverse is true. Likewise, if simple selenium concentration were the critical factor, then people who eat a lot of beef might be expected to be immune from the disease, since beef is the single largest source of selenium in the North American diet!55,56 So since Ganther and Ip had shown that different forms of selenium have widely varying cancer-fighting potencies, might the explanation for the cancer protection provided by these vegetables relate to the kind of selenium that they contain?

It would make sense. Even before Ip and Ganther had zeroed in on SeMC as the superior selenium supplement, it was known that different plants stored the selenium they drew in from the Earth in different biochemical forms.54

When soil selenium is low, most of the selenium in a plant appears as selenate; but as concentrations increase, plants protect themselves against the possible toxicity of inorganic forms of the mineral by storing it in relatively nontoxic forms, such as selenomethionine and SeMC. So if, in high-selenium areas, one plant stored selenium in a form which had a greater cancer-fighting potential, that plant would be more protective than another plant which contained more total selenium in a less effective form.

The hypothesis proved correct. Once again, SeMC provided the key to unlock the mystery – by proving once again its superior anticancer shield.

It turns out that when soil selenium levels are high enough, SeMC is the selenium that dominates in cancer-fighting foods like broccoli, onions, and garlic, while cereal grains and other foods which are not especially linked to reduced cancer risk store most of their “excess” selenium as selenomethionine.57 And in a series of experiments, researchers have shown conclusively that the SEMC in these foods lies behind much of the unique defense against cancer which they provide.

Scientists at the Grand Forks Human Nutrition Research Center designed an ingenious study33 to determine how much of the anti-cancer effects of high-selenium broccoli and broccoli sprouts is attributable to the phytonutrients in these plants, and how much is the result of the kind of selenium which they contain. The researchers exposed six groups of laboratory animals to dimethylhydrazine (DMH), a deadly colon-cancer carcinogen. One group was given a basic, nutritionally-adequate diet. A second group was given the same diet along with a “megadose” selenium supplement in the form of sodium selenite. A third group was given the basic diet along with low-selenium broccoli sprouts. A fourth group ate a diet with the same “megadose” of selenite given to the second group, combined with the low-selenium broccoli sprouts. And the fifth and sixth groups received enough broccoli and broccoli sprouts (respectively) grown in high-selenium conditions to provide the same high dose of selenium as the animals in the “megadose” selenium groups. But while the other animals received their selenium supplement as inorganic selenium, most of the selenium in the diets of animals consuming high-selenium broccoli was SeMC.

You can see the results of this experiment in Figure 3. The colons of animals whose diets were unsupplemented quickly became riddled with precancerous lesions. The phytonutrients in low-selenium broccoli sprouts provided some protection against the formation of these lesions, reducing their numbers by about a quarter. Compared to this, “megadose” inorganic selenium seemed to provide less protection, reducing the burden of abnormal growths by only 16%, but in fact the difference between the two could not be distinguished when analyzed with statistical methods. And indeed, adding the low-selenium sprouts to the “megadose” selenite didn’t actually provide more protection against precancerous lesions than the selenite alone.

Yet high-selenium broccoli or broccoli sprouts, containing the same amount of selenium but mostly in the form of SeMC, slashed the incidence of cancer-forming cells, cutting the burden of precancerous growths roughly in half.33 And this difference was deemed significantly different from all of the other diets – including those with the added low-selenium broccoli foods. Bottom line: the SeMC in high-selenium broccoli and broccoli sprouts plays a greater a role in their anti-cancer effect than their phytonutrients or the absolute amount of selenium!33

Dr. Finley’s group has shown the same effect in breast cancer: the high-selenium broccoli, rich in SeMC, potently lowers the rate of developing early breast cancer lesions – much more effectively than the same dose of selenium as selenate, or of selenite-supplemented broccoli.32,33Likewise, in an animal model of familial adenomatous
polyposis (FAP – an inherited vulnerability to colon cancer), high-SeMC broccoli was dramatically more active in protecting against tumors of the intestines and colon than conventional broccoli, cutting the rate of intestinal tumors by 39%, and massively lowering the risk of tumors in the colon (a 79% reduction!).30

And similar experiments have demonstrated that the same is true of other SeMC-rich vegetables, such as high-selenium garlic,36,58-61 ramps (wild leeks),62 and (to a very limited extent) onions (which don’t accumulate as much SeMC as these other vegetables).60 Whether you compare the selenium in SeMC-rich vegetables to the same amount of selenium from other selenium-enriched foods which do not contain SeMC (such as yeast,58 wheat,31 and even Brazil nuts,60 which are widely famed as a food source for selenium (see Table 2)), or to lower-selenium versions of the same plant, or even to a low-selenium crop plus added selenium from the usual supplemental sources, a high-SeMC diet consistently mounts a better defense against cancer. The inescapable conclusion seems to be that, on the one hand, SeMC, and not simple selenium content, lies behind the protective effects of eating foods from high-selenium soil; and that, on the other hand, the fact that foods like garlic and broccoli produce SeMC (and not other forms, like selenomethionine) is responsible for much of their well-earned anticancer reputation.

So what is it about SeMC – acting through methylselenol – that makes it at once less toxic and more potent as a cancer-fighting selenium supplement?

The Demolitionist and the Arsonist

To answer this question, teams of scientists centered at the AMC Cancer Research Center,25,34-39 the Baylor College of Medicine,40-43 and elsewhere have gone down to the cellular level, exploring the difference between the effects of SeMC on cultured cancer cells and the effects of the forms of selenium found in common selenium supplements. To explain what they’ve discovered, imagine that a cancer cell is an abandoned old tenement tower, rotting from within and in danger of collapsing into neighboring, well-maintained, functional apartments (healthy cells). To protect the people living in the well-maintained apartments, the city administration plans to remove the dilapidated wreck using a clean pulldown process in which the building is collapsed from within, ensuring that its collapse will not damage the surrounding homes.

Now imagine that there is a double threat. The building has been abandoned as hazardous because of its weakened state of repair. But this has made it attractive to a bored gang of youth, who have been on a terror campaign of torching old wrecks for kicks. Of course, indiscriminately setting condemned structures alight may get rid of derelict buildings – but it can also maim or kill innocent people living in the neighborhood if the fire spreads or as the building collapses as its supports burn.

To get to the point of this morality tale: scientists have found that SeMC takes out cancer cells with the precision professionalism of a “demolitions expert,” targeting cancer cells for destruction without harming healthy surrounding tissue. By contrast, regular selenium supplements act, at the cellular level, like an arson gang, killing cancer cells in an inefficient and indiscriminate fashion that inevitably harms healthy cells, too.

Every cell in your body has a “self-destruct button,” like the ones in James Bond’s Aston Martins: a carefully-regulated process known as apoptosis (or “programmed cell death”). The apoptotic “death program” is built into your cells for a variety of reasons: for one thing, it helps the body to get rid of cells which are only needed for brief periods during our development, like the webbing between an embryo’s fingers. But apoptosis is also a critical defense against cancer, allowing the body to automatically shut down cells on the verge of malignant transformation because of DNA damage or the activation of “cancer genes.”

Apoptosis takes malignant cells step by step through a series of well-laid-out stages which
end in its removal – without inflicting damage on surrounding, healthy tissue. The cell’s dysfunctional DNA is fragmented; its mitochondria are shut down; the cell crumples inward and is cleanly consumed by immune cells that home in on the imploding cell.

By studying cancer cells in culture, scientists have demonstrated that SeMC destroys cancer cells through activating the “programmed cell death” of apoptosis:19,35,36,38,40-42,64 it’s the expert demolitionist in the analogy we used above, removing the dangers of a cell
that poses a carcinogenic threat to the body with surgical precision, leaving healthy surrounding tissue unscarred (see Table 3).

But apoptosis is not the only way that cells can be destroyed. Cells can also be laid waste by the ravaging chaos of necrosis. While apoptosis is a carefully-orchestrated process, built into the essence of every cell in your body as a protective self-destruct mechanism, necrosis is the simple vandalizing of the cell by toxins and free radicals.

Necrosis usually begins when a harmful compound agent ruptures cellular membranes, unleashing enzymes present in the cell’s lysosomes (the cellular “garbage incinerators”)
from their carefully-sequestered compartments. These enzymes chew up the cell from within. The cell’s DNA is mutated and otherwise damaged, without being protectively deactivated. The “I-beams” that support the structure of the cell (cytoskeleton) are severed.
Mitochondria swell as they become dysfunctional, like nuclear plants entering meltdown.

In short, when a cell falls prey to necrosis, all hell breaks loose – and it spreads. As the cell bursts, its churning contents trigger an inflammatory overreaction which spreads the havoc of necrosis to surrounding, healthy cells. It’s an ugly, indiscriminate assault, with plenty of innocent bystanders getting caught in the crossfire.

Believe it or not, necrosis is the direct effect of inorganic selenium supplements on healthy and cancerous cells alike (see Table 3). Selenium’s toxicity was recognized long
before its nutritional essentiality was, and the ability of these forms of selenium to kill cancer cells is fundamentally related to their greater toxicity. Compared to healthy cells, cancerous cells are more susceptible to necrotic attack from these more venomous forms of the mineral: in our analogy, they’re like decaying buildings made more vulnerable to fire – tinderboxes filled with fire hazards, just waiting for a spark to set them ablaze. But healthy cells are damaged by inorganic selenium too, either directly (by being poisoned themselves) or indirectly (through the collateral damage inflicted by necrosis and the resulting inflammatory inferno). In the metaphor we used above, conventional selenium supplements are reckless kids playing “pyro” games, engaging in wholesale arson which harms normal cells even as it kills some cancerous ones.

Fortunately, as we’ve seen, the body normally detoxifies some of the selenite or selenate in your diet and supplements by converting it first to hydrogen selenide and then to methylselenol – the same cancer-fighting metabolite formed more directly by SeMC. But the immediate effects of inorganic forms of selenium, and their inefficient conversion into the less-toxic methylselenol metabolite, go a long way toward explaining both their higher toxicity and their lower anti-cancer activity.

From Benchtop to Bottle

As research into the critical role of key selenium metabolites continues, researchers are learning even more about the protective powers of SeMC. They’ve shown how this form of the mineral steps in to shut down the growth of cancer cells early on in their reproductive cycle while conventional forms only become active in the later stages, once the process is already underway.19,34,41,43 And they’ve seen evidence to suggest that, in addition to its direct effects on the tumor, SeMC may also fight cancer by inhibiting angiogenesis,20,27-29 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.

For years, we’ve heard the good news about selenium repeated over and over again – until it seems like an old story. But the SeMC is news that most people haven’t heard, and this selenium story is even more exciting than the early reports. Compared to conventional selenium sources, SeMC is more effective. It’s safer. And it doesn’t build up in your tissues.

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.65 But while the restricted use of SeMC in research laboratories across the United States has brought us some very good news on the selenium front, and can be expected to bring us even more good news in the near future, the fact that you now have the power to choose SeMC as your selenium supplement is, in the end, the best news of all.

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For more information on Selenium, please click below.
Selenium Article 1, Selenium Article 2, Selenium Article 3