Cautionary Tale / Eat Selenium

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What's the p value on selenium being what fixed it
 
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Or don't poop for days.

That seems odd. How do you know it was the Se?

They are good tuna cans with very little PUFA. I don't think you get a lot of PUFA if you drain the can. Tuna is best served fried

It's fat is bound into the muscle tissue, not the water in the can, there's a little in the water sometimes. Fried would be the unhealthiest way to cook it.

.
 

Amazoniac

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but not impossible...
It's a huge complement, isn't it?
Here's something from The Living State:

"An important difference between pure physics and biophysics is in probability.* While physics is the science of the probable, biology is, in a way, the science of the improbable. Probable chemical reactions occur spontaneously. If biological reactions were "probable," they would take place spontaneously, and we would burn up; our machine would run down as a watch relieved of its regulation. Life, on principle, has to work with improbable reactions which it then makes proceed by specific routes, thereby regulating them. Life, altogether, is an improbable phenomenon which was generated, perhaps, but once during the billions of years of the history of the world. If I were to ask a physicist what the probability was that the trillions of electrons and atomic nuclei would get together and stay in the relative position they are in me, the answer would be that the probability was practically zero, which means that I am impossible. One of the main aims of biology is to find out the way in which life makes reactions proceed, thereby perfecting itself.

*Probability has a deep physical meaning. The most probable state of the universe is that of a minimum of free energy and maximum of entropy, randomness. This is the state toward which the universe tends, which makes time flow in its present direction. Once this state is reached, there will be no life."​

--
Regarding selenium, I also noticed benefits from it related to gut function. I experimented multiple times to isolate it, making sure that it wasn't other nutrient that's usually associated with it, like b12, iodine, copper, etc.

Unfortunately the discussion on it is scarce, there are almost no direct associations.
Here's something interesting:
The role of selenium in intestinal motility and morphology in a murine model of Typanosoma cruzi infection
 
Last edited:

Amazoniac

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http://www.traceelements.com/Docs/The Nutritional Relationships of Selenium.pdf
"Ip, reported that the protective effect of selenium on mammary carcinoma in animals was nullified by high vitamin C supplementation.26 Selenium toxicity in laboratory animals is associated with a corresponding decrease in the levels of vitamin C, and vitamin K.27"

"Even though in some circumstances, vitamin C can antagonize selenium, in others it can enhance selenium utilization. Human studies have revealed that vitamin C plays a role in the maintenance of selenium homeostasis.30,31"
 

Amazoniac

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Members that set offices in such ideal conditions that make the outside world unappealing,
One more addition to the discussion:

Selenium in Human Health and Disease
http://www.sbne.org.br/pdf/AC-Selenium-in-human-health-and-disease.pdf

“The essentiality of selenium was demonstrated in the mid-1950s (326), when rats fed a highly purified casein diet developed a fatal liver disease, which was prevented by certain foods, including brewer’s yeast; selenium was identified as the active ingredient (327).”

“A substantial proportion of supplements available contain one species of selenium (mainly in multivitamin/mineral supplements), as selenomethionine, Se-methylselenocysteine, selenite, or selenate. However, selenium-enriched yeast is a complex mixture of several different species of selenium and usually contains more than four different species, including*23%– 84% selenomethionine, 3%–21% selenocysteine, 1%–20% Semethylselenocysteine y-glutamyl Se-methylselenocysteine, 0.5%–5% Se-adenosyl-selenohomocysteine,*4% selenate, plus other selenium species that may vary according to the media and growth conditions of the selenium-enriched yeast (302, 400).”

“The redox-protective effects of selenoproteins may be of particular importance in the thyroid gland, whose long-lived cells generate H2O2 (and so also reactive oxygen species [ROS]) required for the synthesis of thyroid hormones. This likely role is reflected in the abundance of selenium in the thyroid gland (206) and perhaps by the high priority given to maintaining selenium supply to the thyroid gland under conditions where availability is restricted. Also of particular relevance is the direct involvement of selenoenzymes, the iodothyronine deiodinases (DIOs), in thyroid hormone metabolism.”

“A wealth of evidence supports the view that the relative levels of expression of the different DIOs [wiki] in specific tissues and at specific developmental stages or in response to challenges such as tissue injury, illness, and nutritional deficiency is balanced to promote appropriate control of cell proliferation and/or differentiation through control of thyroid hormone activation and inactivation, as reviewed recently (345). For example, compensatory increases in tissue DIO2 activity observed in iodine deficiency or hypothyroidism increased local T3 production (112, 282). Adequate selenium nutrition may thus be particularly important in cases of hypothyroidism to facilitate increased DIO activity in tissues for which the selenium supply is a lower priority than for the thyroid gland.”

“GPx [wiki] activity and expression have been used in many human studies as biomarkers for selenium status (355).”

“Studies in experimental and farm animals indicate that selenium deficiency affects both cell-mediated and humoral components of the immune response (21, 167, 344). In humans, limited data suggest that when intakes of selenium are sub-optimal selenium supplements can enhance immune responses (167). Low serum selenium in humans is associated with low levels of natural killer cells (304), and selenium supplementation (200 mg/day) increased T-lymphocyte-driven tumor lysis and lymphocyte proliferation (200). In rats, selenium deficiency lowers levels of IgA, M, and G; selenium-deficient lymphocytes show lower mitogen-stimulated proliferation, and in cell culture, selenium promotes human neutrophil function (21). Despite these observations the details of how selenium intake influences the immune system remain poorly understood, with the most information being available on the effects of severe selenium deficiency and selenoprotein knockout in response to viral infection.”

“Immune responses are intimately linked to inflammatory processes and these in turn are inter-related to production of ROS and redox control processes. For example, ROS production can increase expression of inflammatory cytokines through increased NF-kB activity (369). It is possible that selenium modulates inflammatory and immune processes through redox functions.”

“White blood cells such as lymphocytes, macrophages, and neutrophils require ROS and pro-inflammatory molecules for their activation, differentiation, and phagocytosis (132). Thus, since selenoproteins may influence these signaling pathways they may in turn be expected to be crucial for these cell functions. For example, neutrophils require oxidative radical production to achieve microbial killing and selenium deficiency lowers the ability of neutrophils to kill ingested microbes, probably partly due to lower GPx1 activity and thus impaired radical metabolism (21). Macrophages are key cells in the signaling and activation of inflammatory responses, but this action also produces ROS; therefore, it must be carefully controlled and counteracted. Studies in which seleniumsupplemented macrophages were stimulated with LPS (a bacterial endotoxin) found that supplementation with selenium suppressed TNF-a and COX-2 (cyclooxygenase-2) expression (386). However, Carlson et al. (79) found that macrophages without any selenoproteins still exhibited normal inflammatory responses, although higher levels of ROS were seen. In a similar experiment, mice with selenoprotein-less T-cells also exhibited increased ROS levels, reduced numbers of mature T-cells, and defective antibody responses (340).”

“Low selenium status has been associated with reduced serum IL6 in elderly people (388), an observation that is consistent with links between selenium, selenoproteins, and inflammatory signaling. In addition to potential metabolic links between GPx1, ROS, and inflammatory cytokines such as the interleukins, results from a series of studies suggest that selenium levels affect eicosanoid metabolism. Studies of both severely selenium-deficient animals and selenium-deficient cells in culture suggest that selenium supply, through its influence on GPxs, has an inhibitory regulatory effect on 50 lipoxygenase activity in lymphocytes (179, 397) and thus on generation of pro-inflammatory leukotrienes. In addition, overexpression of GPx4 in transfected basophils has also been reported to suppress 50 lipoxygenase activity.”

“A combination of severe selenium and iodine deficiency causes a thyroid atrophy that does not respond to iodine supplementation due to inflammatory damage to the thyroid, and this has led to studies of selenium in thyroiditis (205).”

“In summary, there is a growing body of evidence that selenium status affects immune function, in particular the ability to respond to viral infection. The mechanisms underlying these effects are poorly understood but may involve modulation of ROS and inflammatory signaling pathways through the antioxidant and redox functions of selenoproteins.”

“High levels of selenium in diets based predominantly on meat sources appear to be particularly well-tolerated, as exemplified by the high daily selenium intake of the Inuit of North Greenland, estimated as 193–5885 mg (150). This intake results in blood selenium concentrations in the order of 1000 mg /l (300), but is not associated with symptoms of toxicity. Comparison of levels of selenium in blood and urine in the Enshi study population and also in samples from populations in South Dakota (169) revealed toxicity associated with lower concentrations than those that result in symptoms of selenosis in Venezuela (422), probably reflecting exposure to dietary selenium in different forms.”

“The effects of selenium are clearly specific to cancer type and stage (61, 113, 408), and the relative risks and benefits of low/replete/high selenium status should be considered carefully. For example, the NPC trial (86) demonstrated that 200 mg/day selenium-enriched yeast reduced prostate, lung, and colon cancer risk but slightly increased the risk of skin cancer in the cohort who had previously had skin cancer (86). The dose is critical as illustrated by the fact that a relatively high dose of selenium-yeast, 400 mg/day, did not reduce total cancer incidence (303), whereas 200 mg/day selenium-yeast did (86). For selenium and prostate cancer the dose, species, status of the population, and cancer type/grade are all important factors linked to outcome and cancer prevention. From a review of the literature, it seems probable that plasma/serum selenium between >120 and <160 ng/ml may be associated with a protective effect; this level of plasma selenium is normally achieved through consumption of *100– 150 mg selenium/day.”

“In relation to skin cancer, a combined supplement containing selenium-enriched yeast (providing a daily dose of 120mg vitamin C, 30mg vitamin E, 6mg b-carotene, 100 mg selenium and 20mg zinc) was associated with increased incidence, in particular melanoma skin cancer, in women when compared with the placebo group over a follow-up period of *7.5 years in the SU.VI.MAX trial (159). In patients who had a history of skin cancer (nonmelanoma), consumption of 200 mg/day selenium-enriched yeast increased the risk of skin cancer (squamous cell carcinoma and total melanoma skin cancer) compared with the placebo group (86, 102). It seems unlikely that ‘‘optimal selenium status’’ or selenium supplementation regimes can offer protection against skin cancer from the human study data to date and higher selenium status and intakes may be associated with increased risk of skin cancer.”

“A long-term intervention trial in China with selenized table salt fortified with 15 ppm sodium selenite for over 8 years in over 20,000 individuals showed that the incidence of primary liver cancer decreased by 35% in the selenium-supplemented group compared with the control nonsupplemented group (427). Supplementation with selenium-enriched yeast (200 mg/day) reduced the incidence of primary liver cancer in hepatitis B surface antigen-positive individuals compared with the placebo group (427). Hepatitis B viral infection was prevalent in *15% of the population in the Qidong region of China, where this intervention study was completed; those who had hepatitis B had a 200-fold increased risk of primary liver cancer. Selenium reduced the incidence in this population but the exact mechanisms for this protection against liver cancer are not known.”

“Although direct comparisons of odds ratios, hazard ratios (HR), and relative risks for many studies are not possible because the results are study specific, there is a consistent trend throughout several of the human studies demonstrating potential protective effects with plasma/serum selenium between *120–160 ng/ml and reduced risk of some types of cancer when compared with the low plasma selenium status, namely <120 ng/ml. Above 160 ng/ml the cancer protective effect is likely to diminish and the risk perhaps increases for some types of cancer. Literature from the 1950s and 1960s showed that an inappropriately high dose range of selenium may actually increase the incidence of certain types of cancer in animal models and selenium used to be classed as a carcinogen in animals when used at high exposure (84, 334). Therefore, a careful balance ensuring selenium intakes and selenium status fall in the relatively narrow base of the U-shaped risk-response curve is critical for potential modulation of certain cancer-type-specific risk profiles.”

“In addition to being an important antioxidant, selenium has anti-inflammatory properties. The underlying mechanisms have recently been reviewed elsewhere (104). In summary, there are a number of ways in which selenium can influence inflammatory responses, including the inhibition of the NFkB cascade, which induces the production of interleukins and tumor necrosis factor-a (TNF-a) (209). Evidence also suggests that SelS has a key role in inflammatory responses, first identified in diabetic rats (387). Serum amyloid A (SAA) is an acute phase response protein produced in the liver, and SelS has been identified as a potential receptor for the protein (387), thus also establishing a link between selenium and CVD (as SAA is incorporated into HDL cholesterol).”

“Chronic inflammatory disorders are normally associated with a decrease in selenium status, and cross-sectional case–control studies have suggested that patients with inflammatory disorders such as cystic fibrosis (247), acne (246), and inflammatory bowel disease (268) may have a lower selenium status than healthy controls. Therefore, supplementation with selenium could possibly alleviate some of the symptoms of such disorders through increasing antioxidant activity and suppressing inflammatory conditions. Unlike the potential preventative benefits of selenium seen for other health issues, most of the research surrounding inflammatory disorders has been focused on supplementation as an alternative therapy, or treatment, for patients.”

“Miscarriage has also been linked with selenium status; Barrington et al. (30) found that women recently suffering a miscarriage in the first trimester of pregnancy had significantly lower selenium status than pregnant women at the same gestational age. A decrease in antioxidant enzyme activity (particularly the GPxs) is attributed to the effect (428).”

“Behne et al. (38) showed that the testis are a primary target for selenium within the body (Fig. 4), and during times of deficiency the supply of the micronutrient to the male gonads appears to be prioritized. The selenium content of the testis is high, and increases during puberty.”

A summary of their review based on blood levels:
upload_2016-12-24_18-49-6.png
 

Amazoniac

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Forgot to include:
Incidence is referring to the certainty for each aspect investigated. They commented how the possible beneficial range observed on the anti-cancer effect overlaps with the beginning of the problematic effects from another aspect. So, it's a tricky nutrient, and it depends on a lot of things to evaluate how much is right for each person/condition. However, based on the graph, which might not be that reliable, 80-110mcg/d seems like a reasonable range, considering that:
"There is [..] currently some debate as to whether recommendations should be set to prevent overt deficiency symptoms [RDA curve for example] or to maximize optimal health [possible anti-cancer effect curve for example]. This discussion is further fuelled by evidence that suggests that intakes higher than current recommendations may reduce the risk of certain chronic diseases, such as cancer and CVD (see Section VII.A, B). Currently, although many DRI expert bodies acknowledge these relationships, the general conclusion is that the evidence is not sufficient to use for deriving DRI values."

upload_2016-12-24_18-56-8.png
 
Last edited:

papaya

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Members that set offices in such ideal conditions that make the outside world unappealing,
One more addition to the discussion:

Selenium in Human Health and Disease
http://www.sbne.org.br/pdf/AC-Selenium-in-human-health-and-disease.pdf

“The essentiality of selenium was demonstrated in the mid-1950s (326), when rats fed a highly purified casein diet developed a fatal liver disease, which was prevented by certain foods, including brewer’s yeast; selenium was identified as the active ingredient (327).”

“A substantial proportion of supplements available contain one species of selenium (mainly in multivitamin/mineral supplements), as selenomethionine, Se-methylselenocysteine, selenite, or selenate. However, selenium-enriched yeast is a complex mixture of several different species of selenium and usually contains more than four different species, including*23%– 84% selenomethionine, 3%–21% selenocysteine, 1%–20% Semethylselenocysteine y-glutamyl Se-methylselenocysteine, 0.5%–5% Se-adenosyl-selenohomocysteine,*4% selenate, plus other selenium species that may vary according to the media and growth conditions of the selenium-enriched yeast (302, 400).”

“The redox-protective effects of selenoproteins may be of particular importance in the thyroid gland, whose long-lived cells generate H2O2 (and so also reactive oxygen species [ROS]) required for the synthesis of thyroid hormones. This likely role is reflected in the abundance of selenium in the thyroid gland (206) and perhaps by the high priority given to maintaining selenium supply to the thyroid gland under conditions where availability is restricted. Also of particular relevance is the direct involvement of selenoenzymes, the iodothyronine deiodinases (DIOs), in thyroid hormone metabolism.”

“A wealth of evidence supports the view that the relative levels of expression of the different DIOs [wiki] in specific tissues and at specific developmental stages or in response to challenges such as tissue injury, illness, and nutritional deficiency is balanced to promote appropriate control of cell proliferation and/or differentiation through control of thyroid hormone activation and inactivation, as reviewed recently (345). For example, compensatory increases in tissue DIO2 activity observed in iodine deficiency or hypothyroidism increased local T3 production (112, 282). Adequate selenium nutrition may thus be particularly important in cases of hypothyroidism to facilitate increased DIO activity in tissues for which the selenium supply is a lower priority than for the thyroid gland.”

“GPx [wiki] activity and expression have been used in many human studies as biomarkers for selenium status (355).”

“Studies in experimental and farm animals indicate that selenium deficiency affects both cell-mediated and humoral components of the immune response (21, 167, 344). In humans, limited data suggest that when intakes of selenium are sub-optimal selenium supplements can enhance immune responses (167). Low serum selenium in humans is associated with low levels of natural killer cells (304), and selenium supplementation (200 mg/day) increased T-lymphocyte-driven tumor lysis and lymphocyte proliferation (200). In rats, selenium deficiency lowers levels of IgA, M, and G; selenium-deficient lymphocytes show lower mitogen-stimulated proliferation, and in cell culture, selenium promotes human neutrophil function (21). Despite these observations the details of how selenium intake influences the immune system remain poorly understood, with the most information being available on the effects of severe selenium deficiency and selenoprotein knockout in response to viral infection.”

“Immune responses are intimately linked to inflammatory processes and these in turn are inter-related to production of ROS and redox control processes. For example, ROS production can increase expression of inflammatory cytokines through increased NF-kB activity (369). It is possible that selenium modulates inflammatory and immune processes through redox functions.”

“White blood cells such as lymphocytes, macrophages, and neutrophils require ROS and pro-inflammatory molecules for their activation, differentiation, and phagocytosis (132). Thus, since selenoproteins may influence these signaling pathways they may in turn be expected to be crucial for these cell functions. For example, neutrophils require oxidative radical production to achieve microbial killing and selenium deficiency lowers the ability of neutrophils to kill ingested microbes, probably partly due to lower GPx1 activity and thus impaired radical metabolism (21). Macrophages are key cells in the signaling and activation of inflammatory responses, but this action also produces ROS; therefore, it must be carefully controlled and counteracted. Studies in which seleniumsupplemented macrophages were stimulated with LPS (a bacterial endotoxin) found that supplementation with selenium suppressed TNF-a and COX-2 (cyclooxygenase-2) expression (386). However, Carlson et al. (79) found that macrophages without any selenoproteins still exhibited normal inflammatory responses, although higher levels of ROS were seen. In a similar experiment, mice with selenoprotein-less T-cells also exhibited increased ROS levels, reduced numbers of mature T-cells, and defective antibody responses (340).”

“Low selenium status has been associated with reduced serum IL6 in elderly people (388), an observation that is consistent with links between selenium, selenoproteins, and inflammatory signaling. In addition to potential metabolic links between GPx1, ROS, and inflammatory cytokines such as the interleukins, results from a series of studies suggest that selenium levels affect eicosanoid metabolism. Studies of both severely selenium-deficient animals and selenium-deficient cells in culture suggest that selenium supply, through its influence on GPxs, has an inhibitory regulatory effect on 50 lipoxygenase activity in lymphocytes (179, 397) and thus on generation of pro-inflammatory leukotrienes. In addition, overexpression of GPx4 in transfected basophils has also been reported to suppress 50 lipoxygenase activity.”

“A combination of severe selenium and iodine deficiency causes a thyroid atrophy that does not respond to iodine supplementation due to inflammatory damage to the thyroid, and this has led to studies of selenium in thyroiditis (205).”

“In summary, there is a growing body of evidence that selenium status affects immune function, in particular the ability to respond to viral infection. The mechanisms underlying these effects are poorly understood but may involve modulation of ROS and inflammatory signaling pathways through the antioxidant and redox functions of selenoproteins.”

“High levels of selenium in diets based predominantly on meat sources appear to be particularly well-tolerated, as exemplified by the high daily selenium intake of the Inuit of North Greenland, estimated as 193–5885 mg (150). This intake results in blood selenium concentrations in the order of 1000 mg /l (300), but is not associated with symptoms of toxicity. Comparison of levels of selenium in blood and urine in the Enshi study population and also in samples from populations in South Dakota (169) revealed toxicity associated with lower concentrations than those that result in symptoms of selenosis in Venezuela (422), probably reflecting exposure to dietary selenium in different forms.”

“The effects of selenium are clearly specific to cancer type and stage (61, 113, 408), and the relative risks and benefits of low/replete/high selenium status should be considered carefully. For example, the NPC trial (86) demonstrated that 200 mg/day selenium-enriched yeast reduced prostate, lung, and colon cancer risk but slightly increased the risk of skin cancer in the cohort who had previously had skin cancer (86). The dose is critical as illustrated by the fact that a relatively high dose of selenium-yeast, 400 mg/day, did not reduce total cancer incidence (303), whereas 200 mg/day selenium-yeast did (86). For selenium and prostate cancer the dose, species, status of the population, and cancer type/grade are all important factors linked to outcome and cancer prevention. From a review of the literature, it seems probable that plasma/serum selenium between >120 and <160 ng/ml may be associated with a protective effect; this level of plasma selenium is normally achieved through consumption of *100– 150 mg selenium/day.”

“In relation to skin cancer, a combined supplement containing selenium-enriched yeast (providing a daily dose of 120mg vitamin C, 30mg vitamin E, 6mg b-carotene, 100 mg selenium and 20mg zinc) was associated with increased incidence, in particular melanoma skin cancer, in women when compared with the placebo group over a follow-up period of *7.5 years in the SU.VI.MAX trial (159). In patients who had a history of skin cancer (nonmelanoma), consumption of 200 mg/day selenium-enriched yeast increased the risk of skin cancer (squamous cell carcinoma and total melanoma skin cancer) compared with the placebo group (86, 102). It seems unlikely that ‘‘optimal selenium status’’ or selenium supplementation regimes can offer protection against skin cancer from the human study data to date and higher selenium status and intakes may be associated with increased risk of skin cancer.”

“A long-term intervention trial in China with selenized table salt fortified with 15 ppm sodium selenite for over 8 years in over 20,000 individuals showed that the incidence of primary liver cancer decreased by 35% in the selenium-supplemented group compared with the control nonsupplemented group (427). Supplementation with selenium-enriched yeast (200 mg/day) reduced the incidence of primary liver cancer in hepatitis B surface antigen-positive individuals compared with the placebo group (427). Hepatitis B viral infection was prevalent in *15% of the population in the Qidong region of China, where this intervention study was completed; those who had hepatitis B had a 200-fold increased risk of primary liver cancer. Selenium reduced the incidence in this population but the exact mechanisms for this protection against liver cancer are not known.”

“Although direct comparisons of odds ratios, hazard ratios (HR), and relative risks for many studies are not possible because the results are study specific, there is a consistent trend throughout several of the human studies demonstrating potential protective effects with plasma/serum selenium between *120–160 ng/ml and reduced risk of some types of cancer when compared with the low plasma selenium status, namely <120 ng/ml. Above 160 ng/ml the cancer protective effect is likely to diminish and the risk perhaps increases for some types of cancer. Literature from the 1950s and 1960s showed that an inappropriately high dose range of selenium may actually increase the incidence of certain types of cancer in animal models and selenium used to be classed as a carcinogen in animals when used at high exposure (84, 334). Therefore, a careful balance ensuring selenium intakes and selenium status fall in the relatively narrow base of the U-shaped risk-response curve is critical for potential modulation of certain cancer-type-specific risk profiles.”

“In addition to being an important antioxidant, selenium has anti-inflammatory properties. The underlying mechanisms have recently been reviewed elsewhere (104). In summary, there are a number of ways in which selenium can influence inflammatory responses, including the inhibition of the NFkB cascade, which induces the production of interleukins and tumor necrosis factor-a (TNF-a) (209). Evidence also suggests that SelS has a key role in inflammatory responses, first identified in diabetic rats (387). Serum amyloid A (SAA) is an acute phase response protein produced in the liver, and SelS has been identified as a potential receptor for the protein (387), thus also establishing a link between selenium and CVD (as SAA is incorporated into HDL cholesterol).”

“Chronic inflammatory disorders are normally associated with a decrease in selenium status, and cross-sectional case–control studies have suggested that patients with inflammatory disorders such as cystic fibrosis (247), acne (246), and inflammatory bowel disease (268) may have a lower selenium status than healthy controls. Therefore, supplementation with selenium could possibly alleviate some of the symptoms of such disorders through increasing antioxidant activity and suppressing inflammatory conditions. Unlike the potential preventative benefits of selenium seen for other health issues, most of the research surrounding inflammatory disorders has been focused on supplementation as an alternative therapy, or treatment, for patients.”

“Miscarriage has also been linked with selenium status; Barrington et al. (30) found that women recently suffering a miscarriage in the first trimester of pregnancy had significantly lower selenium status than pregnant women at the same gestational age. A decrease in antioxidant enzyme activity (particularly the GPxs) is attributed to the effect (428).”

“Behne et al. (38) showed that the testis are a primary target for selenium within the body (Fig. 4), and during times of deficiency the supply of the micronutrient to the male gonads appears to be prioritized. The selenium content of the testis is high, and increases during puberty.”

A summary of their review based on blood levels:
View attachment 4302
would brewers yeast would be the best way to get selenium???
 

Amazoniac

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Members that have no idea who Paul Vincent I, The Great, is, but are still being part of a future relatable history (something like someone that happened to be passing by when the first plane flew);

Here's a study in which they found that people needed an addition of 50mcg/d to optimize a certain marker that's used as an indicator of optimal selenium levels, which requires a total of about 105mcg/d. It falls within the range supported by the study used for that previous graph.

Establishing optimal selenium status: results of a randomized, double-blind, placebo-controlled trial

“[..]dietary reference values are now focused on optimal health, not just on the prevention of deficiency disorders, and this requires a greater understanding of the reported effects of beneficial/optimal intakes of selenium, the relative merits of different forms of selenium, and the effect of marginal selenium status on health. The anticancer effects of selenium are dose-responsive and form-specific (7), and the levels of selenium intakes and status that correlate with a reduction in cancer risk (7) are greater than those required to optimize plasma glutathione peroxidase (12), which reaches a plateau at a plasma selenium concentration of >70 ng/mL (12).”

“Plasma selenium significantly increased in response to selenium-enriched yeast supplements compared with placebo, but did not significantly change in the group given the equivalent of a daily intake of 50 μg Se from selenium-enriched onion meals compared with the control unenriched onion group. This was likely due to differences in the metabolism of the various forms of selenium in the meals compared with the yeast supplement. The predominant extractable form of selenium in uncooked onions was γ-glutamyl selenium-methylselenocysteine (66%); other identified species included selenomethionine (8.6%), selenocysteine (1.2%), and selenite/selenate (6%) (D Hart, unpublished observations, 2009), which is similar to the species profile reported by Kotrebai et al (34), whereas the main species in the Se-yeast supplement was selenomethionine (60% of total selenium) (22). Selenomethionine, unlike other forms of selenium (19, 30) can be nonspecifically incorporated into plasma proteins (35) and can result in an increase in plasma selenium concentration over a range of intakes (19, 20). Total plasma selenium reflects selenium in the form of selenocysteine, as in the 2 plasma selenoproteins (plasma glutathione peroxidase and selenoprotein P), and also as selenomethionine containing proteins, mainly albumin (35). Because dietary selenomethionine can increase plasma selenium through nonspecific incorporation into plasma proteins, including albumin, but other dietary forms of selenium, including selenocysteine, are metabolized by specific selenium metabolism processes and are not known to be nonspecifically incorporated into plasma proteins (35), this may explain the different response between the 2 groups given 50 μg Se/d from onions or yeast. The effect of selenium-enriched onions on biomarkers of selenium status has not been previously reported.”

“In agreement with other studies (16, 17), we showed that selenoprotein P is a sensitive biomarker for selenium status at low-to-moderate selenium intakes and reflects the intake of selenium present in selenium-enriched food containing various selenium species, unlike plasma selenium, which appears to reflect mainly the selenomethionine content of the food (19). However, in populations with relatively high selenium intakes, selenoprotein P is a less useful as a biomarker (19).”

Suggesting a potential benefit in supplementing in case people are not getting enough from diet alone:
“On the basis of the selenoprotein P data, supplementation with either 50 or 100 μg Se/d as yeast or 50 μg Se-enriched onions/d resulted in improvements in selenium status in a UK cohort with suboptimal selenium status. Only 9% (n = 17) of all volunteers screened for inclusion (n = 182) had a plasma selenium concentration in the putative beneficial range (120–150 ng/mL), and many of these participants (n = 10) regularly took supplements containing selenium. There is a narrow range between deficiency and toxicity; hence, considerable care is required in relation to public health and agricultural policies (eg, entry of selenium into the food chain and use of supplements). The habitual selenium intake of the cohort was estimated to range from 48 to 58 μg/d based on data from the total diet study in the United Kingdom (3), which is similar to the results from a cohort study in Reading, United Kingdom (46). The estimated selenium intake from baseline plasma selenium concentrations (47) was 55 μg/d for the participants recruited into this study.”

Strategies to improve selenium status should focus on dietary advice/modification, and supplements should be avoided by selenium-replete individuals (daily intake >100 μg/d and plasma selenium >130 ng/mL) because they probably provide no additional health benefits. Long-term use of high-dose supplements and high serum selenium concentrations have been associated with an increased risk of diabetes (48, 49) and other adverse effects (48, 50).”

“This study confirms that selenoprotein P is a reliable and sensitive biomarker of selenium status and provides, for the first time, dose-response data that can be used to estimate the selenium intake required to achieve a plateau in plasma selenoprotein P concentrations. Selenoprotein P is involved in the protection against oxidative damage, a reduction in mortality and morbidity from infection (in animal models), the homeostasis and transport of selenium (54) and is associated with a reduction in the risk of morbidity from certain types of cancer (18), all of which provide support for achieving the optimal expression of selenoprotein P. We estimate that an additional 50 μg Se/d is required in addition to the habitual intake (≈55 μg/d) to maximize selenoprotein P concentrations in this 50–64-y-old UK cohort. Considering the other potential health benefits associated with optimal selenium intake and status and the importance of selenoprotein P, the results support an increase in the recommended dietary intake of selenium in adults.”

Something that is often mentioned: since selenium varies a lot depending on the environment, people that eat less processed foods are more likely to obtain suboptimal amounts if the environment doesn't cooperate. Conventional animals products usually provide a decent amount of selenium because the animals are supplemented.
 

David PS

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would brewers yeast would be the best way to get selenium???

I get mine from wheatgrass powder mixed into a glass of water. It is hangover from my green smoothie days. It my not be the best way, but for me it does the trick.

Others have used sodium selenite. You can search for it on the forum.
 

Amazoniac

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Owa, Confessions of a Broken Heart, Rumors are 3 songs by Lindsay Lohan. I hope that this serves as a disclaimer that you should question everything that was posted here. Next time I can leave a Paris Hilton musical disclaimer if it's necessary.

But since no nutrient works in isolation, higher intakes from balanced foods might provide even better general outcomes. As always, the thing is that they have to isolate the nutrient to have a better idea of its effects, but since nutrients interact, it gets to a point where the best outcome from an isolated-type of study is right before it begins to compromise other nutrients significantly, which happens much earlier than the peak of its protective effects for people that are well-nourished. In that previous case, the noticed anti-cancer effects are limited by this dependence/interference, because studies use supplements.
However when you eat the nutrient from natural foods, at least there’s an attempt to incorporate just as much as it can handle, so it’s probably more balanced, and so more supportive.

That’s just to comment that the value of 105mcg/d is safe under those conditions (half diet, half yeast supplement), because if the mean intake from diet of the study was lower (it was 55mcg/d), and assuming that if people ate less selenium they were getting overall less nutrition because nutrients cooperate, then it would be likely that not only the benefits peaked on amounts lower than 105mcg/d (supplements might not be able to compensate for the decrease), but also having to diminish the supplemental amount of 50mcg/d (because the detrimental effects would be perceived earlier as it compromises other nutrients).
In other words, higher selenium intakes from natural foods might be just as or even more beneficial than what was perceived with 105mcg/d.
 
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haidut

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