In the previously referenced article Hashimoto's thydroiditis is mentioned. This is an auto immune disease that I have. I developed it in my early '40s. I gained 20-30 pounds in one month and my Dr. said she would not have diagnosed it except for the fact that I told her that my mother and most of her sisters also have it (she is the oldest of 11, mostly girls).
Bold is mine..
Autoimmune thyroid diseases (AITDs)
AITDs are a form of autoimmune diseases mediated by B and T cells. The two main clinical manifestations of AITDs are Flajani-Basedow-Graves’ disease or Graves’ disease (GD) and Hashimoto’s thyroiditis (HT) [130, 131]. HT led to hypothyroidism by cell-mediated autoimmune destruction, while in GD specific autoantibodies against the thyroid stimulation hormone receptor result in hyperthyroidism [132]. Recent literature shed light on the epigenetic mechanisms involved in the pathogenesis of AITD. DNA methylation, histone modifications, and lncRNA have been deeply analyzed in AITDs. However, the clinical utility of epigenetic modulation still remains elusive. Recent findings confirmed that DNA methylation is also in AITDs setting a very crucial epigenetic mechanism. Global DNA hypomethylation was observed in AITD patients, which may result in overexpressed genes important for a correct immune function, or for the activation of immune cells, ultimately leading into an autoimmune attack towards thyroid tissues [133, 134]. In a genome-wide study, Cai et al. have detected in GD patients more than 200 hyper- and hypo-methylated genetic regions, such as ICAM1, which partly controls cell antigen processing and presentation; DNMT1; and MECP2 genes [133]. Via epigenetic profiling in CD4+ and CD8+ cells from GD patients, hypermethylated gene loci of ICAM1, CD247, and CTLA4 associated with T cell receptor signaling were observed. [133, 134]. Furthermore, hypermethylation of the first intron area in the TSHR gene confirmed that methylation is involved in the development of AITDs. However, DNA hypomethylation levels and susceptibility to AITDs have been correlated to the presence of genetic polymorphisms of DNA methylation-regulatory genes, such as DNMT1 or methionine synthase reductase (MTRR) [135]. Histone modifications play a key role in AITDs, but the exact mechanism(s) in modulating immune tolerance in AITDs is still not fully elucidated. Yan et al. described higher levels of HDAC1 and HDAC2 mRNAs in GD patients thus histone H4 acetylation levels in peripheral blood mononuclear cells of GD patients were lower if compared to those observed in healthy control patient. These results underline the potential importance of aberrant histone modifications in GD patients [24]. In patients with GD, CD4+ and CD8+ cells were presented higher levels of H3K4me3 and H3K27Ac histone marks [134]. IFN-a, an important cytokine secreted during viral infections, has been identified to be able to lead to higher mono and trimethylation levels of H3K4m in thyroid cells [136]. As previously seen for DNA methylation, genetic polymorphism of histone-modifying genes may result in various malfunctions, and/or other further aberrant histone modifications. Sarumaru et al. demonstrated that rs3758391 and rs4746720 in the SIRT1 gene were linked to higher titers of autoantibodies in AITD affected patients [137]. As previously illustrated for other autoimmune disorders, microRNAs actively modulate in various circumstances the differentiation or activation of immune cells and immune response. Two of the most studied miRNA are miR-155-5p and miR-146a-5p, whose overexpression is believed to break immune tolerance thus fostering the development of autoimmune diseases. For example, GD and HT patients exhibit markedly lower levels of miR-155-5p and miR-146a-5p in the thyroid tissues [138]. Although many research’s efforts showed the potential role of other microRNAs, such as miR-125a-3p, miR-197a-3p, miR-22-3p, and miR-183-5p, only a small number of studies investigated their clinical relevance as diagnostic biomarkers [139, 140, 141]. Another epigenetic process called X chromosome inactivation (XCI) has also been discussed in correlation with AITDs [142, 143, 144]. X chromosomes are randomly inactivated in females resulting in transcriptional silencing of one of the X chromosomes [145, 146]. Indeed, AITDs are more often observed in females, confirming the compelling role of XCI in these autoimmune disorders. Brix et al. demonstrated that skewed X chromosome inactivation in female twins with GD and HT was significantly higher than in the control populations, suggesting a probable role of XCI in the etiology of AITD [147]. However, Ishido et al. reported no apparent difference between AITD cases and controls. By contrast, a notable relationship between skewed XCI inactivation and the prognosis of GD and HT was observed [148].
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