HERBS AND SUPPLEMENTS INTRODUCTION HERBS AND SUPPLEMENTS - FEED WHITE BLOOD CELLS (IMMUNE SYSTEM)
SELENIUM (sodium selenite ) 3 capsules, 5 times a day.
HYRANGEA ROOT POWDER (organic germanium), 2 capsules, 5 times a day.
ROSE HIPS (organic vitamin C) 3 capsules, 5 times a day.
RUTIN and Hesperidin in the form of currants contain the organic part of vitamin C. Do not heat them or get them wet. Eat straight, after freezing, 1 tsp x 3. One Tbsp. of peanut butter keeps your WBC supplied with both germanium and selenium for a day. Eat 1-2 Tbsp. daily to be able to stop these supplements for a day. (EDITORS' NOTE; Non-organic peanuts are sprayed with glyphosate -in Roundup - to dry them out, to desiccate them.)
(Hulda Clark, PHD, The Cure and Prevention of All Cancers, p. 385, 2009.)
SELENIUM PART I: SELENIUM - FEED YOUR WHITE BLOOD CELLS
EDITORS' NOTE:
This is the FEED YOUR WHITE BLOOD CELLS' section. Cancer patients have starving white blood cells. Here are some of the items proposed by Dr. Hulda Clark to help feed the white blood cells: SELENIUM, ROSE HIPS, VITAMIN C, and HYDRANGEA. For more about this protocol, go to: http://www.drclark.net/en/cleanses/advanced/white-blood-cells-supplements.
"Selenite, by virtue of oxidizing cell membrane thiols, can prevent the formation of the (tumor) coat and consequently makes cancer cells vulnerable to the immune surveillance and destruction."Boguslaw Lipinski, 2005.
"We showed the unsuitability of selenite to prevent or decrease breast cancer development and mestastasis." Chen CY et al., 2013.
WHAT IS SELENIUM?
"Selenium is a trace element that is naturally present in many foods, added to others, and available as a dietary supplement. Selenium, which is nutritionally essential for humans, is a constituent of more than two dozen selenoproteins that play critical roles in reproduction, thyroid hormone metabolism, DNA synthesis, and protection from oxidative damage and infection." (Seehttp://ods.od.nih.gov/factsheets/Selenium-HealthProfessional/,)
Selenium exists in two forms, inorganic and organic. Inorganic selenium is in the soil that is taken up by plants and converted to the organic forms.
For inorganic selenium, the one form that is used in the studies below is SODIUM SELENITE.
For organic selenium, the two forms that are used in the studies below are METHYLSELENINIC ACID and SELENOMETHIONINE.
But which form or forms of selenium should be used as a supplement? Is sodium selenite a key oxidant in cancer therapy? How about methylseleninic acid and selenomethionine (which is incorporated into methionine in proteins) for cancer?
All sides of selenium strategies are presented.
FOODS RICH IN SELENIUM
BRAZIL NUTS
"Dietary selenium comes from nuts, cereals, meat, mushrooms, fish, and eggs. Brazil nuts are the richest ordinary dietary source (though this is soil-dependent, since the Brazil nut does not require high levels of the element for its own needs). High levels are also found in kidney, tuna, crab, and lobster." (See wikipedia.org.)
SODIUM SELENITE TO PREVENT CANCER
A COOL "RATIONALE" TO USE SELENIUM FOR CANCER - CAN SELENIUM PREVENT TUMOR COAT FORMATION?
We learned in the DIGESTIVE ENZYMES' section that digestive enzymes may be able to digest off the cancer cell's tumor coat.
Can sodium selenite prevent the tumor coat from even forming?
Boguslaw Lipinski, PHD, believes that the power of selenite is as an oxidant.
" .... Selenite is not an antioxidant, but possesses oxidizing properties in the presence of specific substrates." While it was thought that antioxidants would be helpful in cancer, the 'paradox' is that when there is low oxygen in cancerous tissue - hypoxia - there are "reductive rather than oxidative free radicals."
Polythiols (having sulfhydryl {SH} groups) that are "associated with cancer membrane-bound proteins" are seen in cancer cells in a low oxygen state. It is these sulfur and hydrogen compounds that can react with, among other things, fibrinogen, "to form an insoluble and protease-resistant fibrin-like polymer." A tumor coat!
" ,,,,Tumor cells become surrounded by a coat which masks specific tumor antigens, thus allowing cancer cells to escape immune recognition and elimination by natural killer (NK) cells."
"Selenite, by virtue of oxidizing cell membrane thiols, can prevent the formation of the (tumor) coat and consequently makes cancer cells vulnerable to the immune surveillance and destruction."
Yes, according to this neat rationale for using selenium for cancer, selenite can prevent the formation of the cancer cell's tumor coat!
Plus, "... Selenite may directly activate NK cells as well as inhibit angiogenesis without undesirable decrease in the oxidative potential of cellular environment."
(See Lipinski B, Rationale for the Treatment of Cancer with Sodium Selenite, Med Hypotheses, 2005.)
SODIUM SELENITE TO PREVENT CANCER EFFECT OF SELENIUM ON LYMPHOCYTES AND NATURAL KILLER CELLS
What is the effect of dietary selenium on the white blood cells' lymphocytes to kill cancer cells?
After being given alloantigen, study participants, already replete with selenium, were given 200 micrograms of selenium daily for eight weeks to determine if selenium would propel their lymphocytes to transform into cytotoxic lymphocytes to kill cancer cells.
Results? There was an "118% increase in cytotoxic lymphocyte-mediated tumor cytotoxicity and an 82.3% increase in natural killer cell activity as compared to baseline values. This apparently was related to the ability of the nutrient to enhance the expression of receptors for the growth regulatory lymphokine interleukin-2, and consequently, the rate of cell proliferation and differentiation into cytotoxic cells."
Conclusion: "... The immunoenhancing effects of selenium in humans require supplementation above the replete levels produced by normal dietary intake."
(See Kiremidjian-Schumacher L et al., Supplementation with Selenium and Human Immune Cell Functions. II. Effect on Cytotoxic Lymphocytes and Natural Killer Cells, Biol Trace Elem Res, 1994.)
SODIUM SELENITE TO PREVENT CANCER SELENIUM AUGMENTS NK AND LYMPHOKINE-ACTIVATED KILLER CELLS
In another Kiremidjian-Schumacher L et al. study, the researchers evaluated the effects of sodium selenite on the NK cells and lymphokine-activated killer cells (white blood cells stimulated to kill tumor cells) in mice.
Results? After 2.0 ppm for eight weeks of selenium, there was "a significant increase in the lytic (destructive) activity of activated NK cells, and cells from these highly lytic effector cell populations expressed significantly higher numbers of intermediate affinity interleukin-2 receptors cell (cultured in the presence of IL-2 results in effector cells)." In high concentrations of IL-2 and selenium, "spleen NK cells developed into lymphokine-activated killer cells had a significantly enhanced ability to proliferate ... and a significantly augmented cytolytic activity against both NK-sensitive and NK-resistant target cell."
Conclusion: "Selenium appears to enhance the lytic activity of activated NK cells and to augment the proliferation, expansion, and lytic activity of lymphokine-activated killer cells in the presence of high concentrations of IL-2 through its ability to enhance the expression of intermediate affinity IL-2R (receptor) on these cells. (See Kiremidjian-Schumacher L et al., Supplementation with Selenium Augments the Functions of Natural Killer and Lymphokine-Activated Killer Cells, Biol Trace Elem Res, 1996.)
SODIUM SELENITE TO PREVENT CANCER - HAVE A BRCA1 MUTATION? TAKE SELENIUM! SELENIUM NORMALIZES CHROMOSOME BREAKS IN WOMEN WHO ARE BRCA1 CARRIERS
"The mechanism by which selenium reduces the frequency of chromosome breaks in BRCA1 carriers is unclear, but it is likely that selenium reduces the frequency of double-stranded breaks, as opposed to correcting the capacity of the cells to repair broken strands of DNA."
EDITORS' NOTE:: This study is one of our favorite studies!
Can selenium reduce chromosome breaks in BRCA1 carriers?
The BRCA1 gene is involved in repairing double-stranded DNA breaks caused by some cancer-causing agent. When the BRCA1 gene is somehow deficient - mutated - the inability of BRCA1 to repair the double-stranded DNA breaks leads to "an increase in the formation of gross chromosome rearrangements" that can all lead to cancer.
The objective of the Kowalska E et al. researchers in their 2005 study, was to determine if there are any preventive strategies to help BRCA1 carriers fend off cancer. The first step was to find out how BRCA1 carriers respond to a carcinogen, namely bleomycin, "a known mutagenic agent that typically induces double-strand breaks (similar to those induced by ionizing radiation)."
The lymphocytes (white blood cells) of the BRCA1 carriers were cultured in the presence of bleomycin. Similarly, the lymphocytes of non-BRCA1 carriers, who were relatives (many of them sisters), were also cultured in the bleomycin.
Results? "Carriers of BRCA1 mutations showed significantly greater mean frequencies of induced chromosome breaks per cell than did healthy noncarrier relatives (0.58 versus 0.39; P < 10−4)." This is TWICE the chromosome damage of their healthy sisters or other relatives.
Next, the researchers wondered if they could normalize the chromosome breaks. They decided to experiment with selenium.
Why selenium?
Selenium, in the form of selenium selenite (inorganic selenium), in a daily dose of 276 ug (micrograms), was chosen due to its anticancer properties, "including protection against oxidative damage and enhancing nucleotide excision repair." Referenced was the Liu et al study that used selenium selenite to "profoundly" inhibit rat breast cancer in chemically DMBA-treated rats. (Editors' Note - See the Liu study in this section.)
Results? In the BRCA1 carriers,"The frequency of chromosome breaks was greatly reduced following 1 to 3 months of oral selenium supplementation (mean, 0.63 breaks per cell versus 0.40 ... The mean level of chromosome breaks in carriers following supplementation was similar to that of the noncarrier controls (0.40 versus 0.39)."
The rates of chromosome breaks in the BRCA1 carriers normalized! The BRCA1 carriers were now just like their sisters or other relatives!
"The mechanism by which selenium reduces the frequency of chromosome breaks in BRCA1 carriers is unclear, but it is likely that selenium reduces the frequency of double-stranded breaks, as opposed to correcting the capacity of the cells to repair broken strands of DNA."
(See Kowalska E et al., Increased Rates of Chromosome Breakage in BRCA1 Carriers Are Normalized by Oral Selenium Supplementation, Cancer Epidemiol Biomarkers Prev, 2005.)
SODIUM SELENITE TO PREVENT CANCER
CHROMOSOME BREAKS NORMALIZED IN BRCA1 CARRIERS WITH SODIM SELENITE. -DO FEWER CHROMOSOME BREAKS REDUCE RISK, PREVENT CANCER? - ON TO A CANCER PREVENTION STUDY
"Ultimately, it is hoped to show a reduction in breast cancer incidence in BRCA1 carriers associated with selenium supplementation."
Thus, in two pilot studies, Huzarski T et al. in 2006, aimed, "to verify the idea that selenium supplementation of diet reduces the risk of cancer in women with a BRCA1 mutation."
The studies included 200 BRCA1 carriers, 100 matched pairs - cases and controls. Results? "After two years of oral selenium administration the frequency of BRCA1-associated tumors was two times lower in women who supplemented their diet with selenium, as compared to women without supplementation."
(Note that a larger clinical study was ongoing at the time.) (See Huzarski T et al., A Lowering of Breast and Ovarian Cancer Risk in Women with a BRCA1 Mutation by Selenium Supplementation of Diet, Hered Cancer Clin Pract, 2006.)
SODIUM SELENITE TO PREVENT CANCER
SELENIUM PARTLY WEAKENS CADMIUM TOXICITY IN CHICKEN SPLEEN LYMPHOCYTES
Cadmium, found in cigarettes, etc., is a potent environmental toxin.
In their 2015 study, Xu F et al. explored the effects of selenium and cadmium on changes in the gene expression in immune cytokines in the lymphocytes of chicken spleens.
Already, the researchers had found that, "Selenium (sodium selenite) ameliorated the cadmium-induced apoptosis in chicken spleen lymphocytes."
What about the immune cyokine messenger RNA expression in the lymphocytes of chicken spleens after cadmium exposure?
Chicken splenic lymphocytes were divided into selenium, cadmium. and selenium and cadmium only groups with a control group and incubated for 12, 24, 36, 48, and 60 h. Testing was conducted on the messenger RNA levels of interleukin (IL)-1β, IL-2, IL-4, IL-10, IL-17, and interferon-γ. "...The mRNA expression levels of IL-2, IL-4, IL-10, IL-17, and IFN-γ decreased significantly in the cadmium-alone-treated group." Another finding was that. "Levels of IL-2, IL-4, IL-10, IL-17, and IFN-γ in the cadmium and selenium-treated groups were significantly higher than those in the cadmium-alone-treated groups; however, the levels were not as high as the selenium-alone-treated groups and the control group." Note that for IL-1B (an inflammatory cytokine), "The mRNA expression level of IL-1β in the cadmium and selenitum--treated group was lower than in the Cd-alone-treated group." An interesting finding was that, "Cadmium polarized the immune system response to type 2 in cells stimulated via T-cell receptors." With a type 2 immune response there might be cadmium-induced allergies and an impaired ability to inactivate viruses.
Conclusion: "Selenium partly attenuates immune toxicity induced by cadmium in chicken splenic lymphocytes"
(See XuF et al., Effects of Selenium and Cadmium on Changes in the Gene Expression of Immune Cytokines in Chicken Splenic Lymphocytes, Biol Trace Elem Res, 2016.)
SODIUM SELENITE TO PREVENT CANCER
INHIBITING DMBA-INDUCED DNA ADDUCTS AND RAT BREAST TUMORS
The goals of the formative Liu J et al.1996 study were to determine if selenium could inhibit the formation of the chemical, DMBA, from forming DMBA-DNA adducts, and if a decrease in adducts would correlate with fewer rat breast tumors.
A cancer-causing chemical, such as DMBA, can bind to the DNA and start the cancer process. Can selenium stop the initiation of cancer by a toxic chemical? In an effort to thwart the initiation of the cancer process that may be caused by DMBA, the researchers chose to use selenium supplementation in rats.
In one experiment, " ....Selenium, as sodium selenite at 0.1, 0.5, 1, 2, or 4 µg/g were fed for 2 weeks prior to and 2 weeks following treatment with DMBA (5 mg/kg body weight). Results? Tumor incidence correlated inversely to the quantity of selenium consumed. Final tumor incidences were 52, 32, 24, 14, and 10% for rats fed 0.1, 0.5, 1, 2, and 4 µg selenium/g, respectively.
In a separate study, "....In a group of rats fed a diet containing 4 µg selenium/g during both the initiation and promotion stages, the final tumor incidence was 4.8%. Selenite supplementation for 2 weeks markedly depressed the occurrence of individual and total DMBA-DNA adducts. The final mammary tumor incidence correlated positively with total DMBA-DNA adducts."
Conclusion: "These studies clearly demonstrate that selenite can inhibit the initiation stage of mammary carcinogenesis. This reduction in tumor incidence is likely due to a reduction in carcinogen metabolism and ultimately adduct formation."
(EDITORS' NOTE: This study, finding that selenium helped prevent chemically-caused cancer, factored into doing the Kowalska studies above.)
(See Liu J, Inhibition of 7,12-Dimethylbenz(a)anthracene-Induced Mammary Tumors and DNA Adducts by Dietary Selenite, Cancer res, 1997.)
ANOTHER FORM OF SELENIUM - METHYLSELENINIC ACID (MSA) SELENIUM
MODIFIES BONE BUILDING CELLS - OSTEOBLASTS- INFLAMMATORY STRESS RESPONSE TO METASTATIC BREAST CANCER CELLS
If breast cancer metastasizes to the bones and creates osteolytic lesions, it is likely due to cancer-activated osteoclasts (bone cell degradation).
Bisphosonate drugs have been offered to breast cancer patients with bone metastases but, "While this therapy slows lesion progression, the bone does not heal." It is "possible" that the cancer cells "impair the function of osteoblasts, the bone forming cells."
In the Chen YC et al. 2009 study, the researchers found that these bone forming cells, osteoblasts, during breast cancer metastasis to the bones, "increased expression of several pro-inflammatory molecules, such as two interleukins, IL-6, IL-8, and monocyte chemoattractant protein-1 (MCP-1).
"It has long been suspected from both experimental and epidemiological studies that inflammation is strongly linked to cancer." And a key regulatory factor of inflammation is NF-kB.
Since NF-kB regulates the inflammatory cytokines, IL-6 and MCP-1, NF-kB needs to be tamped down.
But how?
Knowing that selenium had previously had an effect on NF-kB activation in macrophages, the researchers decided to use selenium in the form of methylseleniniic acid (MSA) on metastatic breast cancer cells.
The upshot? Selenium in the form of MSA "effectively inhibited activation of NF-kB and subsequently the formation of IL-6, MCP-1, INOS, and COX2."
Furthermore, "Surprisingly to us, short (minute to hour) exposure to MSA was sufficient to suppress the inflammatory response. This result implied that MSA possibly produced short-lived active metabolites. However, during this time, MSA also increased the synthesis of major selenoproteins, GPx1 (glutathione peroxidase) and possibly others. .... Thus, MSA may suppress NF-kB and the osteoblast stress response through metabolites and/or selenoproteins yet to be identified."
The researchers commented: "Metastatic lesions often originate from tumor cells after a long period of dormancy in the target tissue. In breast cancer, tumor cells may disseminate early from non-invasive tumors but remain dormant in the secondary tissue or in the lymph nodes for years. All together, it may be impossible to totally prevent metastasis since it is difficult to define the time or the critical stages of this event. However, reducing the damage from the metastases is still beneficial. Dietary selenium supplementation can increase intracellular selenium levels sufficient to produce useful 'bioactive' intermediates and selenoproteins. By the time dormant micrometastases in the bone begin to proliferate, the higher selenium levels in osteoblasts may prevent or reduce their responses to cancer cells, which in turm may slow the metastatic growth and break the vicious cycle. There are many reports that selenium functions in both cancer initiation and progression. ... In summary, we have demonstrated that selenium supplementation significantly reduced the inflammatory response of ostoblasts to metastatic breast cancer cells by inactivating the nuclear translocation of NF-kB. The expression of NF-kB-dependent genes, which play an important role in metastasis, were downregulated, implying that selenium supplementation may negatively impact the metastasis process."
(See Chen CY et al., Selenium Modifies the Osteoblast Inflammatory Stress Response to Bone Metastatic Breast Cancer, Carcinogenesis, 2009.)
\TO PREVENT BREAST CANCER DEVELOPMENT, METASTASIS IN MICE, WHICH FORM OF SELENIUM - SODIUM SELENITE, MSA, OR SEMET - IS MOST EFFECTIVE?
SELENOMETHIONINE (SeMet) IS MOST EFFECTIVE!! As seen above, The Chen CY et al. group found that methylselininic acid (MSA) "mitigated an osteoblast inflammatory response to cancer cells."
But very few studies have been conducted on the role of selenium in "the later stages of tumor development, including metastasis."
In their 2013 study, the Chen group continued their work with selenium, this time focusing on whether dietary selenium could have an effect on breast cancer development and metastasis in a mouse model.
In their experiments, these researchers fed selenium in three forms - sodium selenite, methylselininic acid (MSA), or selenomethionine (SeMet) - to mice prior to their being inoculated with breast cancer tumor cells. "The primary tumor growth, the numbers of cancer cells present in lungs, hearts, livers, kidneys and femur, and several proinflammatory cytokines were measured.
Results:
"Inorganic selenite supplementation provided only short-term delay of tumor growth."
"The two organic selenium supplements, SeMet and MSA, provided more potent growth inhibition."
"Mice fed selenite developed the most extensive metastasis and had an increased incidence of kidney and bone metastasis.
"...Mice fed the SeMet diet showed the least amount of cancer growth at metastatic sites."
The MSA diet also provided some protection against breast cancer metastasis although the effects were less significant than those of SeMet."
"The cytokine profiles indicated that serum levels of interleukin -2, interleukein-6, interferon y, and vascular endothelial growth factor were elevated in SeMet-supplemented mice."
"Our data suggest that organic selenium supplementation may reduce/delay breast cancer metastasis, while selenite may exacerbate it."
The researchers note that metastasis is associated with a poor prognosis, and circulating tumor cells can indicate that there is metastasis without any clinical symptoms. So, "These findings illustrate the difficulty in determining when metastasis occurs and how to prevent it. One approach may be to use a dietary supplement as a preventive treatment."
The researchers acknowledge that no selenium compound tested was the ":magic cure" for preventing tumors and metastasis. What they found was that sodium selenite only was helpful in a "short-term" delay of tumors, but was "overcome at later stages". By contrast, the two organic selenium compounds, SeMet and MSA, "were more potent in inhibiting primary tumor growth."
Summary: "SeMet supplementation provided more protection from breast cancer metastasis than selenite and MSA supplementations in a mouse model. We showed the unsuitability of selenite to prevent or decrease breast cancer development and mestastasis. Although the selenite diet provided short-term protection against tumor growth, these same mice exhibited extensive metastasis. Our data suggested that the selenite diet may increase breast cancer metastasis to the kidney and to bone. Our results also indicated that organic selenium compounds inhibited tumor growth ore efficiently and had a greater effect on metastasis. An assay of serum cytokines indicated that mice fed SeMet and MSA had higher levels IL-6, IL-2, IFNy, TNFa and VEGF. In particular, SeMet provided the strongest defense against breast cancer development."
(See Chen CY et al., Dietary Selenium Supplementation Modifies Breast Tumor Growth and Metastasis, Int J Cancer, 2013.)
SELENIUM (SODIUM SELENITE), THE MICROBIOTA, AND THE HOST INCREASE OF MICROBIOTA DIVERSITY WITH DIETARY SELENIUM IN MICE
The objective of the Kasalkina MV et al. 2011 study "was to characterize the impact of selenium diets on the microbiota and the role of the microbiota in influencing the selenium status of the host."
The premise is that, "Gut microorganisms, like their hosts, are expected to be sensitive to trace elements."
How about the trace element, selenium?
Background: "Selenium is an essential trace element that plays an important role in human health. In particular, it is required for biosynthesis of selenoproteins, which participate in the regulation of cellular redox homeostasis, protection from oxidative stress, immune response, cancer chemoprevention, and other processes."
Since about one-quarter of all bacteria express selenoproteins, these bacteria require selenium. Interestingly enough, the number of selenoproteins in bacteria can range from 0-57. For example, E.coli has three selenoproteins.
For the bacteria that require selenium, they may sequester, really hoard, selenium, since the bacteria need the selenoproteins for "optimal growth".
The upshot of bacteria grabbing up selenium? "This use of selenium by microorganisms decreases the availability of this trace element for the expression of host selenoproteins. As a result, microbiota increases the requirement of the host for selenium.."
Results Relevant for Bacteria and Host: After experimenting with selenium-deficient, selenium-sufficient, and selenium-enriched mice, the "results indicate that dietary selenium (sodim selenite) can affect both the composition of the existing microbiota and establishment of gastrointestinal microflora. Particularly, in both experiments, the strongest effect was observed within the genus Parabacteroides of the phlylum Bacteriodetes, which demonstrated the opposite correlation with dietary selenium supplementation. ... This finding might be explained by the use of selenium by various microorganisms and selenium toxicity to certain organisms. We also observed differential effects of selenium across multiple phylotypes belonging to the phylum Bacteriodetes. It is possible that the niches vacated by the effect of selenium on Parabacteroides were filled by other phylotypes within related taxonomic groups. The fact that multiple groups showed increases while fewer groups, in general, showed decreases is consistent with the overall effect of selenium on increasing diversity of the microbiota." And, further, "Specific phylotypes showed differential effects of selenium, even within a genus, implying that selenium had unique effects across microbial taxa. Conventionalized germ-free mice (transplanted with flora) subjected to selenium diets gave similar results and showed an increased diversity of the bacterial population in animals fed with higher levels of selenium."
For the germ-free mice expressing selenoproteins, "Germ-free mice fed selenium diets modified their selenoproteome expression similar to control mice but showed higher levels and activity of glutathione peroxidase 1 and methionine-R-sulfoxide reductase 1 in the liver, suggesting partial sequestration of selenium by the gut microorganisms, limiting its availability for the host."
Conclusion - The experiments were " chosen to mimic the dietary selenium intake in the human population. For example, the 0.1-ppm selenium diet approximately corresponds to the human recommended dietary allowance for adults, whereas 0.4 ppm selenium may correspond to the diet supplemented with 200 μg Se/d, which is the dose most often used in human clinical trials involving selenium. In our experiments, the CV (flora transferred to the mice) mice had higher requirements for selenium compared to the germ-free mice, likely due to sequestration of selenium by gut microorganisms, which compete for selenium with the host. These data may also be relevant for understanding the mechanisms of selenium mediated protection against malignant transformation of the colon epithelium, but further studies are required to test this idea."
(See Kasalkina MV et al., Dietary Selenium Affects Host Selenoproteome Expression by Influencing the Gut Microbiota, FASEB J, 2011.)