Association of chronic fatigue syndrome with premature telomere attrition (2018) Unger et al

From the "Conclusions" section of the paper...

This observation of shorter telomeres along with reports of low- or high-grade inflammation mediated by pro-inflammatory cytokines and metabolic decline/mitochondrial dysfunction provide multiple levels of support to include ME/CFS to the list of conditions associated with accelerated aging that could be triggered by genetic, epigenetic, infection, stress or other environmental factors.
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MeSci said:
Could it just mean that the cells are older than usual?
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I'm not sure. Telomeres shorten when cells divide, so it could be argued that older cells, those that have gone through fewer cell divisions, would have longer telomeres (cerebral neurons, for instance, are never replaced). On the other hand, telomere length can reconstitute, so it seems like the decline of that ability may be the major contributor to shorter telomere length.
 
For context to...

This shorter telomere length translates to roughly 10.1-20.5, 4.0-8.2 and 6.6-13.7 years of additional aging in CFS, CFS-X and ISF compared to NF respectively.
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...I would highlight that this week's New Scientist reports a separate study that shows that telomere lengths in women who have children are shorter by an equivalent of 11 years ageing compared to women who are childless. Yet AFAIK mothers don't die 11 years earlier than non-mothers, so I wouldn't over-interpret this data.
 
Forbin said:
Given all that, you might think that telomeres should be lengthening, not shortening, in ME/CFS patients. Mady Hornig's work at Columbia suggested that, on average, the immune systems of ME/CFS patients were "in high gear" early in the disease, but then became "exhausted" later on. I wonder if telomeres might be shortening during an initial phase of unusually high activity, but then reconstituting during a later period of "metabolic suppression."
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We aren't nematodes and we aren't hibernating. Telomere shortening is potentially consistent with chronic illness...
 
Hutan said:
This is an old study now. Has it been replicated?
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Not that I know of. I think I missed it in 2018. Telomere exhaustion is potentially interesting in chronic illness but I am not sure what to make of measurements on white blood cells. Most white blood cells have arisen very recently from stem cell precursors which by definition have endless telomere replacement systems. So they don't reflect 'aging' of the person as a whole. To look at that you would want to look at endothelial cells or fibroblasts maybe. Some white blood cells are older lymphocytes which may lose telomere length but that will be tied up with immune responses, again not ageing.

It might be worth repeating with purified T cells and B cells but even then it would be quite hard to interpret.
 
That's a really interesting comment.

So, could it be that this finding says nothing about aging per se, but hints at white blood cells potentially being, on average older in the people with ME/CFS (and/or having sedentary lifestyles or immune challenges)?
 
I still recall Dr Ros Vallings, medical advisor to ANZMES, standing up at an ANZMES annual general meeting reporting on this study and suggesting that those of us with ME/CFS were going to run out of telomere length before other people and so die earlier. There were children with ME/CFS in the audience. It seemed such an irresponsible thing for anyone, but especially for a doctor, to do on the basis of one study.
 
Hutan said:
I still recall Dr Ros Vallings, medical advisor to ANZMES, standing up at an ANZMES annual general meeting reporting on this study and suggesting that those of us with ME/CFS were going to run out of telomere length before other people and so die earlier. There were children with ME/CFS in the audience. It seemed such an irresponsible thing for anyone, but especially for a doctor, to do on the basis of one study.
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I remember having the exact opposite. Entering a doctors office for the first time with ME. And they spent half the appointment [before I had even gotten a chance to speak myself] speaking about how people with ME have the same life expectancy as healthy people and that I shouldn’t “be anxious”, even though I had never spoken to this doctor before, all they knew about me was that I had ME/CFS because that is what I mentioned when making the appointment. That made me uncomfortable and seemed irresponsible aswell.

Perhaps doctors should stay away from mentioning life expectancy unprovoked until we have more research.
 
Jonathan Edwards said:
Not that I know of. I think I missed it in 2018. Telomere exhaustion is potentially interesting in chronic illness but I am not sure what to make of measurements on white blood cells. Most white blood cells have arisen very recently from stem cell precursors which by definition have endless telomere replacement systems. So they don't reflect 'aging' of the person as a whole. To look at that you would want to look at endothelial cells or fibroblasts maybe. Some white blood cells are older lymphocytes which may lose telomere length but that will be tied up with immune responses, again not ageing.

It might be worth repeating with purified T cells and B cells but even then it would be quite hard to interpret.
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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
 
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