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Unger: Telomere Length Analysis in Chronic Fatigue Syndrome

Bob

Senior Member
Messages
16,455
Location
England (south coast)
I think this might be old research (?), and it's only a conference poster abstract, but it's a new publication, so here it is...


Telomere Length Analysis in Chronic Fatigue Syndrome
ER Unger, J Murray, LP Oakley, JM Lin, MS Rajeevan.
April 2016
The FASEB Journal vol. 30. no. 1. Supplement lb459
http://www.fasebj.org/content/30/1_...ted-by=yes&legid=fasebj;30/1_Supplement/lb459
This abstract is from the Experimental Biology 2016 Meeting. There is no full text article associated with this abstract published in The FASEB Journal.
Abstract

Background
Chronic fatigue syndrome (CFS) is a severely disabling condition associated with multi-system symptoms including marked post-exertional malaise, fatigue, pain, unrefreshing sleep and cognitive impairment. The symptoms and risk factors share features with accelerating aging. Aging and a variety of metabolic, inflammatory, infectious and neoplastic conditions have been associated with accelerated telomere attrition. This analysis was performed to evaluate whether CFS shares this association.

Methods DNA was isolated from 705 PAXgene whole blood samples from 751 participants in the 2007–09 follow-up of the Georgia CFS Surveillance study who completed the clinical evaluation used to identify exclusionary medical and psychiatric conditions that could explain fatigue. Using the 1994 CFS Research Case Definition with questionnaire-based subscale thresholds for fatigue, function and symptoms, participants were classified as: 1) CFS if all criteria met (n=71); 2) CFS-X if CFS with exclusionary conditions (n=78); 3) Insufficient Symptoms/Fatigue (ISF) if only some criteria met, regardless of exclusionary conditions (n=340); 4) Non-Fatigued (NF) if no criteria met and no exclusionary conditions (n=212;47 NF participants with exclusions were not included and 3 could not be classified). Relative telomere length was measured using real-time PCR. Telomere specific primers generate a signal proportional to total sum of the length of all telomeres in the sample (T). Telomere signal is normalized to signal from primers to single-copy gene (S). The T/S ratio is proportional to average telomere length per cell. T/S is expressed relative to reference DNA, assigned T/S of 1.0. Conversion of T/S to Southern blot hybridization determination of terminal restriction fragment telomere length in base pairs (bp) was based on data from 20 healthy volunteers tested by both methods. Linear and logistic models were used to examine association between CFS, T/S ratio and covariates. Level of significance was set at p < 0.05. This analysis concerned 639 participants with telomere, classification and co-variate data: 77 CFS-X, 64 CFS, 302 ISF, and 196 NF.

Results Age (48.04 ± 0.38 years) did not differ across groups, but obesity, sex, race, education and income, significantly differed. T/S ratios ranged from 0.269 to 4.138. When comparing T/S ratios across groups, telomere lengths were significantly shorter in CFS and ISF than NF (CFS: 0.93±0.03, ISF: 0.94±0.02; NF: 1.09±0.04). These differences remained significant after adjusting for covariates (age, BMI, waist-hip-ratio, education, and sex). Based on adjusted group means, telomere length was shorter by 212, 593 and 508 bp in CFS-X, CFS and ISF compared to NF. As expected there was a significant negative correlation between telomere length and age in the study sample overall. NF subjects started with long telomeres but shortened at a faster rate (59 bp/year) than the rate of telomere shortening in CFS-X (25.4 bp/year), CFS (21.2 bp/year) and ISF (4.2 bp/year).

Conclusions Our results indicate that CFS should be included in the list of conditions associated with telomere shortening. Further work is needed to evaluate if the shortening has functional significance in CFS.
 

alex3619

Senior Member
Messages
13,810
Location
Logan, Queensland, Australia
This makes sense, sadly. Some extreme event, probably getting ME but we cannot be certain as this event might be what creates a risk for ME, massively shortens telomere length. Then we have lower metabolic rate, so continual shortening proceeds slowly.

This research is still in the early phase. The finding might be adjusted with more data.

We also do not know if that patient group is properly characterized, and I do not have the cognitive energy to go back through the research.
 

alex3619

Senior Member
Messages
13,810
Location
Logan, Queensland, Australia
Well, that sounds shitty :p

I`m just gonna go ahead and presume that they get long again with treatment.
One of the downsides, if this proves right, is that life expectancy, which is not that good anyway, is likely to go down if we get better. Quality, not quantity. However I doubt it will go down much. For example: 2000 days of quality life versus 2010 days of poor life experience ... its a no-brainer.

(For those who are younger than me, its probably more like 10,000 days of good life, versus 10,050 of illness.)
 

Marky90

Science breeds knowledge, opinion breeds ignorance
Messages
1,253
One of the downsides, if this proves right, is that life expectancy, which is not that good anyway, is likely to go down if we get better. Quality, not quantity. However I doubt it will go down much. For example: 2000 days of quality life versus 2010 days of poor life experience ... its a no-brainer.

(For those who are younger than me, its probably more like 10,000 days of good life, versus 10,050 of illness.)

Ah, so telomere shortening is irreversible? This an area I know nothing about, so pardon my norwegian.
Why do you think it would be days less, not years less, with regards to life expectancy?
 

M Paine

Senior Member
Messages
341
Location
Auckland, New Zealand
Ah, so telomere shortening is irreversible? This an area I know nothing about, so pardon my norwegian.
Why do you think it would be days less, not years less, with regards to life expectancy?

Telomere shortening is a failsafe mechanism to prevent cells from dividing too many times. Each time a cell creates a copy of it's DNA, a part of the Telomere sequense at the end of the genome is lost. Certain cells express Telomerase, which allows them to regenerate Telomeres. These are cell lines which can potentially reproduce ad infinitum.

If a cell is of a lineage that does not express telomerase, and has a shortened telomere, it tells you that the cell has replicated a fair amount. One mutation cancer cells can use to become malignant is to express telomerase.

You would increase the risk of introducing mutations leading to cancer if you artificially lengthened telomeres, allowing cells to continue dividing. In a healthy person, short telomeres are a sort of way to know what cells are not good candidates for replication.

I hope this makes sense
 

alicec

Senior Member
Messages
1,572
Location
Australia
Ah, so telomere shortening is irreversible

Not necessarily. When telomerase is active, as it is in stem cells, the telomere shortening that occurs with each cell division is reversed and the cell stays young.

Activating telomerase in other cells is a holy grail of anti-ageing and/or reversal of degenerative disease.

There is an interesting book by Michael Fossel "The Telomerase Revolution" which gives good background and summary of current knowledge and research. He also has a blog.

There is one telomerase activator available commercially. It is quite expensive and Fossel says it is weak. Potentially better ones are in the pipeline - or so it is claimed.
 

M Paine

Senior Member
Messages
341
Location
Auckland, New Zealand
> Activating telomerase in other cells is a holy grail of anti-ageing and/or reversal of degenerative disease.

Probably a quicker path towards activating oncogenes too
 

alicec

Senior Member
Messages
1,572
Location
Australia
Probably a quicker path towards activating oncogenes too

Well Fossel would disagree with that.

I honestly haven't had the energy or sufficient interest to go into the detail but Fossel maintains that if we can reset telomeres (ie considerably lengthen them), then this is protective against cancer.

He does say that attempting to reset telomeres when cancer is already present is much more problematic. One would like to inhibit telomerase in the cancer cell and so ensure that the cell dies.

I find his ideas interesting and certainly a source of optimism. What might come out of it is another question.
 

alex3619

Senior Member
Messages
13,810
Location
Logan, Queensland, Australia
Ah, so telomere shortening is irreversible? This an area I know nothing about, so pardon my norwegian.
Why do you think it would be days less, not years less, with regards to life expectancy?
I have no specific reason, its just that a shortage of telomere length that was very great would result in a lot more cell death. Its also relative to our current situation ... once we are cured the telomere shortening would, if the data is right, accelerate back to normal.

There is a lot of research into fixing telomeres. Its likely they will find way to do it in time.

Telomeres, iirc, are like twist ties at the end of chromosomes so they do not unravel. If you run out of twist ties then the chromosomes can degrade. This happens more and more in advanced age. However this is a bit misleading as it involves limitations of the DNA repair mechanism, and in this analogy the telomeres would be scaffolding the repair crew can hang onto, but only for repairs at the end of the chromosomes ... I think. Its been 14 years since I studied this stuff, and a lot would have been learned in that time.
 
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Skippa

Anti-BS
Messages
841
Oh effing great.

Guess I'll just go and spend my pension now then, won't be needing it...
 

msf

Senior Member
Messages
3,650
The study says that the non-fatigued group´s telomeres started off longer but shortened quicker than the CFS group. So they sort of catch us up in old age? Ah, good old schadenfreude...

I´ve said sometimes that having mild ME is like being old before your time.
 

Jonathan Edwards

"Gibberish"
Messages
5,256
I am unclear about exactly how to interpret this. However, if these re blood cells derived from stem cells with telomerase then it would seem all that is being measured is the number of divisions between stem cell and mature blood cell. That might change if bone marrow haemopoietic environment changed - maybe altering the number of divisions to get to a mature blood cell. It might also reflect how many old B and T lymphocytes were knocking around in the blood that perhaps should have been apoptosed a while back. I am not sure that this tells us anything about telomere exhaustion in any tissues that might matter, like endothelium, which may die off in scleroderma because of telomere exhaustion.

One of the problems I see with all these studies on blood cells is that the cells in blood are just the ones that happen to be trucking through at that time. Exercise and rest and coffee and all sorts of other things can alter the rate at which cells go in or out. It may be a bit like rummaging through your garbage bins - it may depend on the season or the day of the week what you find.
 

*GG*

senior member
Messages
6,389
Location
Concord, NH
Oh effing great.

Guess I'll just go and spend my pension now then, won't be needing it...

I'm only 40 something, but have retirement money set aside, but thinking the same thing! Have no income, about 2.5 years now waiting upon my Lawyer!

GG
 

barbc56

Senior Member
Messages
3,657
I don't have a clear understanding about telomeres but found this article. If I'm reading this right, this area of study has the potential to be used in mind body research before it's proven that telemere length can be used as a marker to determine the validity of these type of studies.
There is a strong push to make telomere length the currency of how we think, measure, and do science about our health and well-being, and how we target our health interventions. Strong efforts are made to attach the science of telomeres to urgings that we take up yoga, meditation, and “being there” to save our lives.esearch
https://www.sciencebasedmedicine.or...e-scientific-and-pseudoscientific-literature/

I'm curious what others take on this and/or if it's even related to the above study.
 
Messages
15,786
If I'm reading this right, this area of study has the potential to be used in mind body research before it's proven that telemere length can be used as a marker to determine the validity of these type of studies.
I think the article is rather demonstrating that telomeres have the potential to be abused by quacks in their research or claims they're making. It's fairly well accepted that short telomeres are a bad thing (they protect the actual genetic code further down the line), but suggesting that stress-relief slows the shortening of telomeres is just a new form of psychobabble.

As the article points out, the study used to support that claim was not controlled, and other more directly physiological interventions were also included, such as diet and exercise.

I think the basic message is that telomeres are as vulnerable to psychobabble as any other biological concept. It doesn't make telomeres meaningless, it just means we need to continue to scrutinize BS mind-over-body research even when impressive terminology and otherwise valid concepts are mentioned.

It's not really relevant to the Unger study discussed above. Basically that one is just looking at telomere length, not impact of an intervention upon telomere length. Though it may lead to that - but it can still be done responsibly and intelligently.
 

Waverunner

Senior Member
Messages
1,079
Telomere shortening is reversible! We live in wonderful times, don't we :) Lizz Parrish did exactly what I have been proposing over and over again. The current drug approval process is completely flawed, it destroys innovation and creates monopolies because it requires too much money and time to get a drug approved. Hence, be a free human being and decide yourself if you want to take a risk or not. She went abroad and together with a partner started a new company that uses gene therapy to translate latest research findings into actual treatments. George Church is in their advisory board. Lizz used gene therapy on herself to prolong her telomeres and according to latest tests it is working. Her telomeres lengthened by about 20 years, from 6.71 kb to 7.33 kb. BioViva could be the first company to radically change healthcare. Here is an article from four days ago.

http://www.dailymail.co.uk/sciencet...ly-carried-anti-ageing-treatment-herself.html
 

*GG*

senior member
Messages
6,389
Location
Concord, NH
Telomere shortening is reversible! We live in wonderful times, don't we :) Lizz Parrish did exactly what I have been proposing over and over again.

The current drug approval process is completely flawed, it destroys innovation and creates monopolies because it requires too much money and time to get a drug approved. Hence, be a free human being and decide yourself if you want to take a risk or not.

She went abroad and together with a partner started a new company that uses gene therapy to translate latest research findings into actual treatments. George Church is in their advisory board. Lizz used gene therapy on herself to prolong her telomeres and according to latest tests it is working. Her telomeres lengthened by about 20 years, from 6.71 kb to 7.33 kb. BioViva could be the first company to radically change healthcare. Here is an article from four days ago.

http://www.dailymail.co.uk/sciencet...ly-carried-anti-ageing-treatment-herself.html

Yeah, that is what I read, multiple sources (Life Extension and Reason magazine). Maybe it is time for major reforms? Not saying no Regulation! But most people are to timid from the scare- mongering, they are fine with the status quo. Until they get sick and there quality of life suffers, or death is knocking on the door!

GG