BastiFuntasty
Member
- Joined
- Jun 9, 2015
- Messages
- 225
What wasn't understandable?
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What wasn't understandable?
It was, it's just that I didn't find any relevant result..What wasn't understandable?
You are probably right.It was, it's just that I didn't find any relevant result..
Or don't poop for days.
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
Based on toiled evidence, log(1.1..).What's the p value on selenium being what fixed it
Based on toiled evidence, log(1.1..).
Improbable entity?thats pboy value
Improbable entity?
It's a huge complement, isn't it?but not impossible...
would brewers yeast would be the best way to get selenium???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
I'm still too naive to comment on that..would brewers yeast would be the best way to get selenium???
would brewers yeast would be the best way to get selenium???