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Could HDAC inhibitors be bad for undermethylators?

methylation curcumin sulforaphane hdac

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#1 j87

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Posted 20 October 2017 - 08:02 PM

Could this explain why some report that sulforaphane helps with depression and cognitive function, while others report that it makes them worse? 
In this lecture by William Walsh, he mentions that undermethylators should "suppress acetylation of histones" while overmethylators should "support acetylation of histones with folic acid and niacinimide (powerful deacetylase inhibitor)."
Sulforaphane, curcumin, and butyrate are HDAC inhibitors.
Does this mean sulforaphane and curcumin are bad for undermethylators?

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#2 Silverstudy

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Posted 04 May 2018 - 12:53 AM

 Some information I found from a study I was reading.

(While our data supports a role for diet in the epigenetic regulation of heart health, our findings are translatable to other epigenetic diseases including cancer. Indeed, small molecule HDAC inhibitors Vorinostat and Romidepsin are currently approved by the US Food and Drug Administration (FDA) for the treatment of advanced cutaneous T cell lymphoma[1022], with more HDAC inhibitor monotherapy and combination therapy trials currently underway according to clinicaltrials.gov. Current nutrigenomic studies have demonstrated the importance of diet as chemopreventative and chemotherapeutic. More specifically, flavonoids have been identified as chemotherapeutic agents; these studies demonstrate that chemotherapeutic actions of flavonoids work in part by regulating histone modifications via alterations in acetylation and/or methylation [422]. Compounds highlighted in this report including epigallocatechin gallate (EGCG), kaempferol, quercetin, luteolin and apigenin (Fig. 1Table 1), have been shown to regulate multiple post-translational marks that include methylation and acetylation in order to block cancer proliferation and metastasis or promote cancer apoptosis [22]. With regards to our findings, EGCG, kaempferol, quercetin, and apigenin have previously been shown to regulate the Zn-dependent HDACs [12829]. We report for the first time pan-HDAC inhibition by myricetin (Table 1), which has previously been shown to act as an anti-proliferative agent for the treatment of cancer [3031]. Thus, we would speculate that anti-carcinogenic actions of myricetin are mediated in part through HDAC inhibition. In addition to myricetin, we report new evidence that flavonoids, baicalein, baicalin, dihydromyricetin, morin hydrate and myricitrin (Fig.3&4Table 1&2) also inhibit Zn-dependent HDAC activity as well as which HDACs these compounds target (Table 2). Combined, our findings uncover newly identified flavonoid HDAC inhibitors; thus, future examination of these dietary compounds in the epigenetic regulation of cancer prevention, cardioprotection and other disease states would be of significant interest to the field of nutrigenomics.)


L. D. Godoy, J. E. Lucas, A. J. Bender, S. S. Romanick, B. S. Ferguson, 2017, "Targeting the epigenome: Screening bioactive compounds that regulate histone deacetylase activity"   Mol. Nutr. Food Res. 2017, 1600744.


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