Selenocysteine or Selenomethionine should both be good. Look for minimal additives.
Oddly enough currently selenium makes me feel worse even though I know I'm probably deficient.
sara n. said:
Basically: What are the safest supplements to continue using/best ones to wean off of. I only really asked about: Thryoid, VA, VD, VE, VK, Aspirin, Niacinamide.
Most supplements contain enough impurities to eventually cause problems. Thyroid and aspirin are among the safest, and the most likely to be valuable indefinitely.
It depends on where you live, but vitamin D3, vitamin K, and selenium deficiencies are extremely widespread.
I:"For someone taking a supplement, how many times a week should a 200mcg pill be taken to restore t4 conversion, presuming adequate protein?"
Ray:"During the first week, every day would be o.k., then I think once or twice a week is enough."
- Animals foods, such as kidney and shellfish, which deliver selenium primarily as selenocysteine, are probably the safest sources of selenium. Very high intakes of selenocysteine by the Greenland Inuit were not found to be toxic.14
- Plant foods, which deliver selenium primarily as selenomethionine, are probably less safe; selenomethionine is less useful to humans and may be toxic in ways that selenocysteine is not. For instance, selenomethionine supresses the NA repair15 and distorts the NA methylation;16 it also replaces methionine in proteins such as albumin with unclear effects. High levels of selenomethionine intake in people of the Lower Tapajós River of the Amazon Basin in Brazil cause 42 percent of the population to display fingernail damage and 24 percent to have irritation or fungal infections on the skin - both symptoms of selenosis.17
- Inorganic forms such as sodium selenite or selenate, which are commonly found in supplements, are the most dangerous. Developing embryos are sensitive to selenite poisoning: in zebrafish, excess selenite induces loss of neurons from brain, trunk and tail, defects in heart function, and embryonic death, but supplementation with folic acid can relieve the cardiac and neuronal defects.18
The current reference daily intake is 55 μg/d for a healthy adult in the US (30), and the supranutritional dose will be 300–600 μg/d for a healthy U.S. adult if we extrapolate these experimental animal data (12, 28–30). Thus, we think that these doses are physiologically achievable in humans.
The p53 tumor suppressor gene was selected for this study, because it is commonly found to be mutated or differentially methylated in colon cancer and other cancer types (18, 19, 35). It is well recognized that alterations in DNA methylation of certain tumor suppressor genes may be the leading mechanism by which anticancer nutrients exert their action (20, 36).
[..]our present finding that dietary SeMet induced exon-specific DNA hypermethylation of the p53 but not the β-actin gene in a Se dose-response manner is extremely important in both liver and colon mucosa and has several biological implications. It has been documented that breaks in genomic DNA within exons 5–8 of the p53 and exons 2–3 of the β-actin gene are associated with hypomethylation, and genomic DNA stability within this region is directly correlated with hypermethylation (38, 39). Therefore, dietary SeMet may increase the genomic p53 DNA stability, which is critical to prevent DNA mutation, and may subsequently reduce the risk of colon cancer and its metastasis to the liver.
It is also important to know that exon-specific DNA methylation of the p53 gene in rats fed the S[upranutritional] diet was significantly greater than that in rats fed the D[eficient] diet (but not those fed the A[dequate] diet).
In this study, we found that the A and S diets were equally effective at maintaining Se-enzyme activities and the plasma homocysteine concentration, but the S diet resulted in higher tissue Se concentrations than the A diet. In addition, rats fed the S diet had lower global genomic DNA methylation in liver than those fed the D diet. More importantly, our data demonstrated that exon-specific DNA methylation of the p53 gene but not the β-actin gene was dose dependently increased by dietary Se in rat liver and colon mucosa, which may relate to the anticancer action of dietary Se.
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