There will be no more posts on WordPress..Matt Mullenweg apparently does not much care whether WordPress is trolled by vicious, lying ass trolls or is easily fooled.
There is no point in taking liposomal vitamin C. Dehydrosacorbic acid, not acorbic acid, is deficient in many diets, heavily laden with polyphenols, from coffee, tea and sodas, for example, and antioxidant supplements.
I am not recommending this but some iron sulfate taken with vitamin C could increase levels of dehydroascorbic acid. As vitamin C increases iron absorption and as iron is required by the gut supplemental iron would still have to be taken away from vitamin C. When supplementing with iron always tests of iron levels are required.
There is kind of scurvy due to deficiencies of dehydroascorbic acid which is transported by glucose transporters.. There is enough ascorbic acid to prevent vitamin C deficient scurvy. Ascorbic acid is transported by sodium-dependent vitamin C transporters The full panoply of scurvy symptoms is missing but there can be terrible back aches and neck aches. At least some of this new form of scurvy could be due to heavy ingestion of antioxidants especially taken when vitamin C is taken. Antioxidants can reduce dehydroascorbic acid to ascorbic acid.
Finding very easy, safe treatments is very difficult. For back pain and/or neck pain taking 1 gram of vitamin C once a day away from other antioxidants, food, coffee, tea, sodas and/or iron could lead to a significant lessening of pain. I think if one is taking a lot of antioxidants throughout the day one can develop a kind of scurvy due to reduction of dehydoascorbic acid, which is transported by glucose transporters, to ascorbic acid, which is not transported by glucose transporters. There is a huge vitamin C other antioxidants interaction where the interaction is very unfavorable.
N-acetyl-L-cysteine and vitamin C are frequently taken together, however, the two supplements should never be taken together. One of the selling points of taking the two supplements together was that N-acetyl-L-cysteine would prevent the oxidation of vitamin C to dehyrdroascorbate which N-acetyl-L-cysteine very effectively does. However dehyrdroascorbate is the form of vitamin C absorbed via glucose transporters. Preventing the oxidation of vitamin C with N-acetyl-L-cysteine is a huge error. There are many grounds for not supplementing N-acetyl-L-cysteine. The high effectiveness of N-acetyl-L-cysteine in preventing oxidation of vitamin C is one.
Current wisdom holds there is no schizophrenia rather there are multitudes of schizophrenias. Basically current wisdom holds that in any diagnostic category there are multitudes of illnesses with different etiologies rather than single illnesses
I would argue that all mental illnesses arise due to epigenetic dysregulalions of TET enzymes, JmjC domaining containing proteins and dysregulation of acetyl-coenzyme A synthesis which can dysregulate histone acetylation. There is only a single mental illness.. There are many, many expressions of the single mental illness due to epigenetics. Various epigenetic dysregulations channel other epigenetic dysregulations giving rise to distinct illnesses. The same treatment could work for all mental illnesses though only subsets of the treatment could be needed for some illnesses.
This is actually quite a hopeful time in research on mental illness. But any breakthroughs likely will not come from psychiatry but rather arise from basic research which is so often the case. TET enzymes and the gut are huge research interests and those are the two areas that have to be researched for there to be a breakthrough.
I have been arguing that sodium-dependent transporters are dysregulated in epigenetic illnesses. The sodium-dependent vitamin C transporter (SVCT) could be dysregulated in epigenetic illnesses. Dedydroascorbic acid, which is oxidized vitamin C, is transported by glucose transporters. With the SVCT dysregulated dedydroascorbic acid must be available to be transported by glucose transporters.
Taking antioxidants with vitamin C could reduce any dedydroascorbic acid that is produced to ascorbic acid. Vitamin C must then not be taken with other antioxidants such as selenium, coffee or tea. Vitamin C would also not be taken with carbohydrates or sugar as glucose could competitively inhibit the transport of vitamin C by glucose transporters. Fat soluble antioxidant supplements, such as vitamin E and carotenoids should not be taken in much more than RDA amounts as fat soluble antioxidants could reduce dedydroascorbic acid to ascorbic acid throughout the day. A selling point of vitamin E has been that vitamin E reduces oxidized vitamin C but as it turns out this is a very large negative. With vitamin C inside cells due to transport of dedydroascorbic acid into cells by glucose transporters TET enzymes could start working which would hopefully re-regulate SVCTs.
Little is known about the relationship between treatments for bipolar disorder (BD), their therapeutic responses and the DNA methylation status. We investigated whether global DNA methylation levels differ between healthy controls and bipolar patients under different treatments. Global DNA methylation was measured in leukocyte DNA from bipolar patients under lithium monotherapy (n = 29) or combination therapy (n = 32) and from healthy controls (n = 26). Lithium response was assessed using the Alda scale. Lithium in monotherapy was associated with hypomethylation (F = 4.63, p = 0.036). Lithium + valproate showed a hypermethylated pattern compared to lithium alone (F = 7.27, p = 0.011). Lithium response was not associated with DNA methylation levels. These data suggest that the choice of treatment in BD may lead to different levels of global DNA methylation. However, further research is needed to understand its clinical significance.
My take – In bipolar patients not on medications there could be a global DNA hypomethylation. Whether lithium results in global DNA hypomethylation, there is a pre-existing global DNA hypermethylation in bipolar disorder or both is not clear from this research.
Introduction: Hypermethylation of genes associated with promoter CpG islands, and hypomethylation of CpG poor genes, repeat sequences, transposable elements and intergenic genome sections occur during aging in mammals. Methylation levels of certain CpG sites display strict correlation to age and could be used as “epigenetic clock” to predict biological age. Multi-substrate deacetylases SIRT1 and SIRT6 affect aging via locus-specific modulations of chromatin structure and activity of multiple regulatory proteins involved in aging. Random errors in DNA methylation and other epigenetic marks during aging increase the transcriptional noise, and thus lead to enhanced phenotypic variation between cells of the same tissue. Such variation could cause progressive organ dysfunction observed in aged individuals. Multiple experimental data show that induction of NF-κB regulated gene sets occurs in various tissues of aged mammals. Upregulation of multiple miRNAs occurs at mid age leading to downregulation of enzymes and regulatory proteins involved in basic cellular functions, such as DNA repair, oxidative phosphorylation, intermediate metabolism, and others.p
Conclusion: Strong evidence shows that all epigenetic systems contribute to the lifespan control in various organisms. Similar to other cell systems, epigenome is prone to gradual degradation due to the genome damage, stressful agents, and other aging factors. But unlike mutations and other kinds of the genome damage, age-related epigenetic changes could be fully or partially reversed to a “young” state.
My take – Increasing activity of TET enzymes could reduce incidences of cancer, slow aging and ameliorate various mental illness, such as schizophrenia. Increasing activity of TET enzymes can be done now.
Cancer genomes are characterized by focal increases in DNA methylation, co-occurring with widespread hypomethylation. We show that TET deficiency in diverse cell types (ESCs, NPCs, HSCs, pro-B cells, and T cells) results in a similar methylation landscape, with the expected localized increases in DNA methylation in active euchromatic regions, concurrently with unexpected losses of DNA methylation, reactivation of repeat elements, and enrichment for single-nucleotide alterations primarily in heterochromatic compartments. Thus, TET loss of function may be a primary mechanism underlying the characteristic pattern of global hypomethylation coupled to regional hypermethylation observed in diverse cancer genomes. Our data potentially explain the synergy between DNMT3A and TET2 mutations in hematopoietic malignancies, as well as the recurrent association of TET loss of function with cancer.
Cancer genomes are characterized by focal increases in DNA methylation, co-occurring with widespread hypomethylation. Here, we show that TET loss of function results in a similar genomic footprint. Both 5hmC in wild-type (WT) genomes and DNA hypermethylation in TET-deficient genomes are largely confined to the active euchromatic compartment, consistent with the known functions of TET proteins in DNA demethylation and the known distribution of 5hmC at transcribed genes and active enhancers. In contrast, an unexpected DNA hypomethylation noted in multiple TET-deficient genomes is primarily observed in the heterochromatin compartment. In a mouse model of T cell lymphoma driven by TET deficiency (Tet2/3 DKO T cells), genomic analysis of malignant T cells revealed DNA hypomethylation in the heterochromatic genomic compartment, as well as reactivation of repeat elements and enrichment for single-nucleotide alterations, primarily in heterochromatic regions of the genome. Moreover, hematopoietic stem/precursor cells (HSPCs) doubly deficient for Tet2 and Dnmt3a displayed greater losses of DNA methylation than HSPCs singly deficient for Tet2 or Dnmt3a alone, potentially explaining the unexpected synergy between DNMT3A and TET2 mutations in myeloid and lymphoid malignancies. Tet1-deficient cells showed decreased localization of DNMT3A in the heterochromatin compartment compared with WT cells, pointing to a functional interaction between TET and DNMT proteins and providing a potential explanation for the hypomethylation observed in TET-deficient genomes. Our data suggest that TET loss of function may at least partially underlie the characteristic pattern of global hypomethylation coupled to regional hypermethylation observed in diverse cancer genomes, and highlight the potential contribution of heterochromatin hypomethylation to oncogenesis.