Epigenetics, Telomeres and ME/CFS

Chandelier

Senior Member (Voting Rights)
Disclaimer: I‘m brainfoggy and can’t really research the topic in depth.
I might also use wrong vocabulary.
Please bear with me.

My motivation for creating this thread stems from trying to better understand this quote by JE:
Epigenetics is a pretty meaningless buzzword that has become popular which does not correspond to any recognisable epidemiological category. Its use is a neat illustration of just how dumbed down medical science has become. It is often used to imply something in addition to environmental and not genetic but in the context of processes downstream of both.

I’m trying to get a basic understanding of whether there’s a part of epigenetics as a science field that is well grounded in good research.
My understanding is that epigenetics describes that genes can be turned on/off by environmental factors.
And there seem to be different views on what is considered to be part of these environmental factors.

A very biopsychosocial view likes to mention nobel prize winner Elizabeth Blackburn’s research into how stress might affect the length of the protective telomeres.
According to this research, stress (like living with a violent spouse) can result in shortened telomere length.
Studies suggest that chronic psychological stress may accelerate ageing at the cellular level. Intimate partner violence was found to shorten telomere length in formerly abused women versus never abused women, possibly causing poorer overall health and greater morbidity in abused women. 31
But the telomere length hypothesis seems to face skepticism:
I looked this up, and for anyone interested this review: "Telomere Length as a Marker of Biological Age: State-of-the-Art, Open Issues, and Future Perspectives - PMC" goes through the evidence for the usefulness of leukocyte telomere length (LTL) as a marker of biological age, and seems to take a fairly skeptical stance towards it, for instance stating "Furthermore, LTL is largely dependent on the blood-sample leukocyte composition. In addition, it is still not clear whether LTL is a reliable surrogate marker for TL changes in other body tissues". But it also goes through some evidence that indicates it may be a meaningful biomarker too
This skepticism might also be the reason why Blackburn, psychological stress and its proposed impact on telomeres are mentioned on the german epigenetics wikipedia page but are non-existent on the english version.

Excerpt from the german epigenetics wikipedia page:
Psychische Belastung kann die Aktivität dieses Enzyms verringern, was zu einer beschleunigten Verkürzung der Telomere im Alterungsprozess führen kann (Nobelpreis für Medizin 2009 an Elizabeth Blackburn).
Translation:
Psychological stress can reduce the activity of this enzyme, which can lead to an accelerated shortening of telomeres during the aging process (2009 Nobel Prize in Physiology to Elizabeth Blackburn).

In general, I’m wondering why Elizabeth Blackburn’s name doesn’t pop up more often in this forum?
After all, she seems to offer the perfect argument for BPS proponents to make the link between psychological stress and ME/CFS.
She also seems to propose much the same BPS counter-measurements. From her Wikipedia page:
Blackburn comments on ageing reversal and care for one's telomeres through lifestyle: managing chronic stress, exercising, eating better and getting enough sleep; telomere testing, plus cautions and advice. 34
In recent years Blackburn and her colleagues have been investigating the effect of stress on telomerase and telomeres with particular emphasis on mindfulness meditation.
 
I’m trying to get a basic understanding of whether there’s a part of epigenetics as a science field that is well grounded in good research.

Epigenetics is just the study of changes in DNA that do not involve changes in the nucleotide base sequence of the genes as such. Changes of this sort are going on all the time every day, in responses to food, temperature, exercise and in cell maturation from stem cells and all sorts of other things.

However, the term tends to be used to imply changes that get stuck over long periods - even across generations in plants it seems. That includes things like methylation of DNA bases - which alters whether or not the gene can be read.

There is lots of good science around this but there is also a lot of loose talk around disease mechanisms invoking 'epigenetics'.

It all depends on what you are actually interested in, really. 'Epigenetics' isn't to my mind a very useful holdall concept because it covers so many different things occurring at different times and rates. It might even be used to cover long term changes in parts of cells other than DNA - like synpases in neurons. Arguably all adaptive immune responses reflect epigenetic changes. I think the word just confuses.

The suggestion by Blackburn does not seem to go very far. If 'stress' (an even more vague concept) leads to more rapid aging that doesn't help explain ME/CFS, which isn't like more rapid aging.
 
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