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Epigenetic Alterations in Women with Fibromyalgia

  [ 2 votes ]   [ 3 Comments ] • September 28, 2013

Note: You may read the full text of this article free HERE.

Editor's Comment:  “Epigenetics literally means "above" or "on top of" genetics. It refers to external modifications to DNA that turn genes "on" or "off." These modifications do not change the DNA sequence, but instead, they affect how cells "read" genes.” (from  For more information about epigenetics, including examples, see this article at

Epigenetic alterations and an increased frequency of micronuclei in women with fibromyalgia.

By Victoria Menzies, et al.


Fibromyalgia (FM), characterized by chronic widespread pain, fatigue, and cognitive/mood disturbances, leads to reduced workplace productivity and increased healthcare expenses.

To determine if acquired epigenetic/genetic changes are associated with FM, we compared the frequency of spontaneously occurring micronuclei (MN) and genome-wide methylation patterns in women with FM (n = 10) to those seen in comparably aged healthy controls (n = 42 (MN); n = 8 (methylation)).

  • The mean (sd) MN frequency of women with FM (51.4 (21.9)) was significantly higher than that of controls (15.8 (8.5)) (χ (2) = 45.552; df = 1; P = 1.49 × 10(-11)).

  • Significant differences (n = 69 sites) in methylation patterns were observed between cases and controls considering a 5% false discovery rate.

  • The majority of differentially methylated (DM) sites (91%) were attributable to increased values in the women with FM.

  • The DM sites included significant biological clusters involved in neuron differentiation/nervous system development, skeletal/organ system development, and chromatin compaction.

  • Genes associated with DM sites whose function has particular relevance to FM included BDNF, NAT15, HDAC4, PRKCA, RTN1, and PRKG1.

Results support the need for future research to further examine the potential role of epigenetic and acquired chromosomal alterations as a possible biological mechanism underlying FM.

Source: Nursing Research and Practice, 2013. By Victoria Menzies, Debra E. Lyon, Kellie J. Archer, Qing Zhou, Jenni Brumelle, Kimberly H. Jones, G. Gao, Timothy P. York, and Colleen Jackson-Cook. Virginia Commonwealth University School of Nursing, 1100 East Leigh Street, Richmond, VA 23298-0567, USA.

Please Discuss This Article:   Post a Comment 

thanks but
Posted by: roge
Sep 28, 2013
that is nice and all but can we please find some better treatments for FM
Reply Reply

Thank You very much for showing this study.
Posted by: IanH
Sep 28, 2013
What a great study. It shows just how deep this illness goes. I would like to see the same study done on people with ME. Some of the genes involved will be slightly different but some will be the same. I do suspect the elevated levels of micronuclei will be similar. Also the aberrant methylation should show up similarly.

Treatment! Well it does point us in a direction of nutritional epigenetics. Current treatments are hopeless.

In the nutritional field, epigenetics is very important, because nutrients can affect the expression of genes at the transcriptional level. Folate, B-12, methionine, choline, and betaine can affect DNA methylation and histone methylation through altering 1-carbon metabolism.

Two metabolites of 1-carbon metabolism can affect methylation of DNA and histones: S-adenosylmethionine (AdoMet)5, which is a methyl donor for methylation reactions, and S-adenosylhomocysteine (AdoHcy), which is a product inhibitor of methyltransferases.

Other water-soluble B vitamins like b7, b3, and b5 also play important roles in histone modifications. B7 (biotin) is a substrate of histone biotinylation. B3 (niacin) is involved in histone ADP-ribosylation as a substrate of poly(ADP-ribose) polymerase as well as histone acetylation as a substrate of Sirtuin1, which functions as histone deacetylase (HDAC).

NAD-dependent protein deacetylase links transcription regulation directly to intracellular energetics and participates in the coordination of several separated cellular functions such as cell cycle, response to DNA damage, metabolism, apoptosis and autophagy. It modulates chromatin function through deacetylation of histones and can promote alterations in the methylation of histones and DNA, which leads to transcriptional repression. It deacetylates a broad range of transcription factors and coregulators, thereby regulating target gene expression positively and negatively

Pantothenic acid is a part of CoA to form acetyl-CoA, which is the source of acetyl group in histone acetylation.

Some food components directly affect enzymes involved in epigenetics. Eg, genistein and tea catechin affects DNA methyltransferases. Resveratrol inhibits HDAC and curcumin inhibits histone acetyltransferases (HAT).

There is plenty to do now with your treatment. No cure sure but you can influence your FM by increasing the substrates that control methylation.
Reply Reply

Posted by: BlackBeltw/Fibro
Nov 20, 2013
Let's take it one step deeper and consider the possibility that due to genetic defects FM patients may not be able to absorb nutrients from birth.
Reply Reply

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