4 replies to this topic

[GreenPower]

Here's a new study referenced which shows how the length of telomeres changes during the development of cancer. It might be interesting in this forum due to the previous speculations on the correlation between telomere lengths and the risk for cancer.

 

The study, which is the first to track telomere changes over years in people developing cancer, was published in EbioMedicine.

 

"Understanding this pattern of telomere growth may mean it can be a predictive biomarker for cancer," Dr. Lifang Hou, the lead study author and a professor of preventive medicine at Northwestern University Feinberg School of Medicine, said in a statement. "Because we saw a strong relationship in the pattern across a wide variety of cancers, with the right testing these procedures could be used to eventually diagnose a wide variety of cancers."

For years, scientists have been trying to understand the relationship between telomeres, considered a marker of biological age, and cancer development. Previous results, however, have been inconsistent.

In the new study, researchers looked at the measurements of telomeres in 792 people over the course of 13 years. Of these participants, 135 were eventually diagnosed with different types of cancers, including prostate, skin, lung, leukemia and others.

Initially, scientists gathered that telomeres aged more quickly - indicated by a more rapid loss of length - in the individuals who were developing cancer. In these people, the telomeres appeared as much as 15 years older than those who were not developing the disease. The study also found that the accelerated aging of the telomeres stopped three to four years before the individuals were diagnosed with cancer.

This is believed to be the first study to explore telomere length at more than one point in time before cancer diagnosis. Cancer treatment may shorten telomeres so it is uncertain how their length is affected by cancer itself or the treatment.

Researchers say this is likely why previous studies have been so inconsistent. "We saw the inflection point at which rapid telomere shortening stabilizes," Hou said. "We found cancer has hijacked the telomere shortening in order to flourish in the body."

[Steve H]

Further evidence IMO to suggest longer Telomeres do provide Cancer protection and that Telomere therapy would be a valid anti aging intervention. I suspect the Telomere Positioning Effect is contributing to increasing levels of instability as aging genes are activated by Telomere attrition (Shay and Wright), this then leads into Epigentic drift giving Cancer a chance to hijack the cells. I have never been more convinced that Telomere length is a primary driver of aging and systemic dysfunction and not just a simple replication clock as some people consider them. 

[Alpharius]

I would be nevertheless careful with drawing conclusions which implicate direct causality instead of correlation. Read: People who get cancer develop shorter telomeres before. Short telomeres can contribute to higher cancer rate, but it could be some kind of stress which does simultaneously reduce telomere length and also initiates cancer formation (dependent and independent of telomeres).

[Steve H]

Alpharius you make a good point though in any case Telomere attrition is implicated as a contributor to various aging pathology and consequences. I think Dr Fossel is correct that intervention upstream on Telomeres could very well help Epigenetically recover the aged phenotype in the cells as has been seen in various experiments. I certainly think its one of the few avenues likely to result in robust rejuvenation that we can deliver now as an immediate intervention into aging. 

 

Dr Fossel recently had this to say about Telomerase activation:

 

Many of you have asked about Helen Blau’s work at Stanford, using telomerase mRNA [FASEB Journal]. Helen sent me a copy of her article when it came out and I’m a serious fan of her work. As some of you know from my upcoming book, The Telomerase Revolution, there are four approaches to resetting telomeres: 1) put in a new telomerase gene, 2) activate the telomerase gene that is already in cells, 3) put in the mRNA (as Helen’s group did) for telomerase, or 4) put in the telomerase protein itself.

 

The first problem with mRNA is that the molecule is incredibly fragile and has a short half-life at body temperature, making it hard to work with in the lab (in vitro) and even harder to work with in patients (in vivo). The second problem (with both mRNA and protein) is that you only get one copy of the final telomerase enzyme, whereas if you put in the gene or activate the gene, you get multiple copies of the enzyme and a lot more “bang for your buck”. In short, mRNA is great, but has a low ROI, clinically speaking. The third problem, a recurrent one in this field, is that if you read either Helen’s paper or the slew of media articles and interviews since publication, the emphasis is always on treating “genetic disease” (such as one of the muscular dystrophies) rather than “aging disease” (such as Alzheimer’s). There is an unspoken and almost universal assumption that genetic diseases like the various muscular dystrophies are “real”, but aging diseases like Alzheimer’s aren’t true “diseases” at all, but they “just happen because things wear out”. This common assumption leads most researchers to focus on inherited genetic conditions exclusively and completely ignore normal aging processes and their associated clinical pathology – such as Alzheimer’s. Even when researchers DO focus on Alzheimer’s they operate on the assumption that it must involve a “bad gene” (such as APOE4).

 

Both assumptions are false, but are shared by most of the academic and medical research community, even if neither assumption is ever clearly stated or acknowledged. Since researchers “know” that aging is not a classic genetic disease, they are equally complacent in thinking that aging diseases cannot be treated by a genetic approach. The result is that almost no one approaches aging diseases in a practical way, using fundamental interventions such as telomerase mRNA, telomerase activation, telomerase protein, or – as in our case at Telocyte – telomerase gene therapy.

 

Bioviva proposes to attempt approach 1) put in a new telomerase gene, hopefully the community here will help support this so we can move the needle on intervention. 

[TaiChiKid]

There was a very large scale recent study on telomere length as well.  Here is a blog about it:  http://joshmitteldor...-and-mortality/

 

The actual study is written up here:  http://jnci.oxfordjo.../6/djv074.short

 

 

Some highlights:

 

    This new Danish study puts this theory to rest.  At last there is enough data that corrections can be made for smoking, obesity, exercise, and all major life style variables that could conceivably be have an impact on mortality comparable to the large effect we find associated with telomere length.

    The correction is done using a statistical method called ANOVA, which can partition the causes of mortality into statistical bins and say how much is due to smoking, how much is due to blood cholesterol, how much is due to age, and how much is due to telomere shortening.

 

Results from the study:

•     Impact of telomere length on mortality, raw data:   3.38 (meaning that the 10% of people with the shortest telomeres were dying at a rate 3.38 as high as the 10% with the longest telomeres)
•     Same calculation, corrected for age:  1.54
•     Same calculation, corrected for age and all other hazard variables:  1.40

Conclusion: This demonstrates that age is the biggest factor in mortality, and telomere length has a strong effect, independent of age.  All the health variables together are a small factor compared to age and telomere length.

 

Short telomeres are not just a marker but a major cause of mortality.

 

Evolution has turned telomerase off such that short telomeres substantially affect our life span.  Turning telomerase on would not have cost anything, but that is not what evolution has done.

 

So the theory is wrong that says evolution has already made our life spans as long as possible.  Evolution has arranged for us to age and die “on purpose”.  Withholding telomerase is part of an evolved death program.