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

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hixxy

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J Transl Med. 2018 Feb 27;16(1):44. doi: 10.1186/s12967-018-1414-x.

Association of chronic fatigue syndrome with premature telomere attrition.

Rajeevan MS, Murray J, Oakley L, Lin JS, Unger ER.

Abstract

BACKGROUND:
Chronic fatigue syndrome (CFS), also known as myalgic encephalomyelitis (ME), is a severely debilitating condition of unknown etiology. The symptoms and risk factors of ME/CFS share features of accelerated aging implicated in several diseases. Using telomere length as a marker, this study was performed to test the hypothesis that ME/CFS is associated with accelerated aging.

METHODS:
Participant (n = 639) data came from the follow-up time point of the Georgia CFS surveillance study. Using the 1994 CFS Research Case Definition with questionnaire-based subscale thresholds for fatigue, function, and symptoms, participants were classified into four illness groups: CFS if all criteria were met (n = 64), CFS-X if CFS with exclusionary conditions (n = 77), ISF (insufficient symptoms/fatigue) if only some criteria were met regardless of exclusionary conditions (n = 302), and NF (non-fatigued) if no criteria and no exclusionary conditions (n = 196). Relative telomere length (T/S ratio) was measured using DNA from whole blood and real-time PCR. General linear models were used to estimate the association of illness groups or T/S ratio with demographics, biological measures and covariates with significance set at p < 0.05.

RESULTS:
The mean T/S ratio differed significantly by illness group (p = 0.0017); the T/S ratios in CFS (0.90 ± 0.03) and ISF (0.94 ± 0.02) were each significantly lower than in NF (1.06 ± 0.04). Differences in T/S ratio by illness groups remained significant after adjustment for covariates of age, sex, body mass index, waist-hip ratio, post-exertional malaise and education attainment. Telomere length was shorter by 635, 254 and 424 base pairs in CFS, CFS-X and ISF, respectively, compared to NF. 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. Further, stratified analyses based on age and sex demonstrated that the association of ME/CFS with short telomeres is largely moderated by female subjects < 45 years old.

CONCLUSIONS:
This study found a significant association of ME/CFS with premature telomere attrition that is largely moderated by female subjects < 45 years old. Our results indicate that ME/CFS could be included in the list of conditions associated with accelerated aging. Further work is needed to evaluate the functional significance of accelerated aging in ME/CFS.

KEYWORDS:
Chronic fatigue syndrome; Immunosenescence; Myalgic encephalomyelitis; Stress; Telomere attrition
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https://www.ncbi.nlm.nih.gov/pubmed/29486769
https://translational-medicine.biomedcentral.com/articles/10.1186/s12967-018-1414-x
 
Not sure I want to know I'm ageing faster than normal. Interesting research, but I wonder what if any implications it has for treatment, or for helping with understanding more about what's really going on in our bodies, and why.
 
MeSci said:
Have any studies been done that find pwME look about 10 years YOUNGER than their age?
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The odd thing is the people who tell me this most often are doctors and nurses. I had this happen about two weeks ago when a nurse I'd never seen before looked at me strange and then had me verify my name and my age, at which points she said "Wow, you sure don't look your age." I even had an ophthalmologist once tell me during an examination, "My goodness, you have the retinas of a teenager." I should have said, "Yes, but he wants them back by 5 o'clock."
 
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Forbin said:
The odd thing is the people who tell me this most often are doctors and nurses. I had this happen about two weeks ago when a nurse I had had never seen before looked at me strange and then had me verify my name and my age, at which points she said "Wow, you sure don't look your age." I even had an ophthalmologist once tell me during an examination, "My goodness, you have the retinas of a teenager." I should have said, "Yes, but he wants them back by 5 o'clock."
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Me too. On good days, I look about 20 years younger than my birth age. Maybe it’s because I mostly stay out of the sun?
 
I suspect that getting very little sun might slow some of the appearances of ageing.

We're not a hard living lot generally.

There are also definitely a lot of strains related to ill health though. I wonder if this teolmere finding (assuming it's not just a fluke) represents something that might provide information on the cause of ME/CFS, or is more likely to be some secondary issue.

About five years ago I remember seeing a lot of people complain that research on telomeres and ill-health/life problems/anxiety/etc was being over-hyped.
 
I know 80-90 year olds with way more energy/verve/active life than I, so yeah, defo prematurely aging on the inside.
Had a doctor years ago suggest that telomere attrition was an issue for me, but of course there was no solution so I promptly forgot all about it.
 
Elizabeth Unger MD PhD. "Chief of the Chronic Viral Disease Branch (CVDB), Division of High-Consequence Pathogens and Pathology, National Center for Emerging and Zoonotic Infectious Diseases at the Centers for Disease Control & Prevention."

I saw Dr. Unger at the 2017 Invest in ME conference in London. I wonder if she'll be attending or possibly presenting this year?

http://me-pedia.org/wiki/Elizabeth_Unger
 
Esther12 said:
I suspect that getting very little sun might slow some of the appearances of ageing.

We're not a hard living lot generally.
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Even in my mid-20's people assumed I was about 10 years younger. In my early 30's a dentist perplexed me by scolding me for having the teeth of a 30 year old :confused:

That was all before I got sick. And I lived in rural Oklahoma for a couple years (lots of playing & working outside) and then Hawaii in high school. Had to avoid burning, but there was no lack of sun exposure :cool:
 
If I shave (rare event these days) it easily takes ten years off. Mostly because my beard is about 80% white these days.

Also, like Sasha, I have basically stayed indoors or under shade all my adult life.
 
I think I spent quite a lot of time outside both in good and bad weather throughout my life, including since I got ME. I used to get very sunburned/tanned, and still do a bit, but can't tolerate heat (or cold) so much now.
 
If we are hypometabolic, doesn't that mean our metabolism is slower, therefore we would age slower and look younger?

Anyway, FWIW, this blogger talks about Rapamune as an anti-aging medication.

"It is the particular action of inflammation against healthy, native tissues that is arguably the greatest source of metabolic damage in aging, and rapamycin may offer a particular protection against this destruction."

I'm currently taking Rapamune off-label for ME and have some improvement. He mentions other potential benefits...and side effects.

https://joshmitteldorf.scienceblog.com/2016/06/13/rapamycin-redux/
 
ScottTriGuy said:
If we are hypometabolic, doesn't that mean our metabolism is slower, therefore we would age slower and look younger?
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That sounds sort of logical, but if our metabolism is slower, that presumably means necessary processes like cell repairs may happen slowly too and malfunctions be more likely to occur, leading to faster ageing. I have no idea whether that makes any sense biochemically.
 
Webdog said:
Elizabeth Unger MD PhD. "Chief of the Chronic Viral Disease Branch (CVDB), Division of High-Consequence Pathogens and Pathology, National Center for Emerging and Zoonotic Infectious Diseases at the Centers for Disease Control & Prevention."

I saw Dr. Unger at the 2017 Invest in ME conference in London. I wonder if she'll be attending or possibly presenting this year?

http://me-pedia.org/wiki/Elizabeth_Unger
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Yes, she is presenting at the conference this year: http://investinme.eu/IIMEC13-news-180104.shtml

We are are now enormously pleased to announce that the USA Centers for Disease Control and Prevention (CDC) will also be represented at both Colloquium and Conference.

Dr Elizabeth (Beth) Unger will be presenting at both BRMEC8 and IIMEC13.

This is the second year running that the CDC will be present at our events - though last year Dr Unger did not have the opportunity to present at the Conference .

Elizabeth Unger PhD, MD Chief, Chronic Viral Diseases Branch Division of High-Consequence Pathogens and Pathology National Center for Emerging and Zoonotic Infectious Diseases, Atlanta, GA. More: http://investinme.eu/IIMEC13-news-180104.shtml
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In Osler's Web, Dr. David Bell is described as having noticed that his patients, and the patients of other ME doctors, had a "numb" and unchanging set of facial features that was characteristic of them. He called their faces "bland" and "lacking the vitality of expression." Called "myopathic facies," the condition is seen in other diseases, such a myasthenia gravis, and is described as an "inability to curve the corners of the mouth, due to muscle weakness."

Holding an unusually neutral expression (something I've been accused of) might be a subconscious reaction to a disease in which every exertion makes you feel worse.

If this persisted over a lifetime, I could imagine that it might make you look younger than you actually are simply because it would promote less creasing of the face. That, in combination with less sun exposure, might explain a lot.
 
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I thought this passage from the "telomere" wikipedia page was interesting in that it mentions hibernation and C. elegans.

The bolding below is mine.
It is becoming apparent that reversing shortening of telomeres through temporary activation of telomerase may be a potent means to slow aging. The reason that this would extend human life is because it would extend the Hayflick limit. Three routes have been proposed to reverse telomere shortening: drugs, gene therapy, or metabolic suppression, so-called, torpor/hibernation. So far these ideas have not been proven in humans, but it has been demonstrated that telomere shortening is reversed in hibernation and aging is slowed (Turbill, et al. 2012 & 2013) and that hibernation prolongs life-span (Lyman et al. 1981). It has also been demonstrated that telomere extension has successfully reversed some signs of aging in laboratory mice [40][41] and the nematode worm species Caenorhabditis elegans.[42]
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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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